- 1 Should you wait to drink water after taking Zofran
- 2 What do I do if I throw up right after taking Zofran
- 3 Does water help or worsen nausea
- 4 How long after eating can I take Zofran
- 5 Can you drink after taking anti nausea medicine
- 6 Why do I still feel sick after taking Zofran
Should you wait to drink water after taking Zofran
How to use Zofran ODT 8 Mg Disintegrating Tablet – This medication is dissolved on top of the tongue, It is not meant to be chewed or swallowed like other tablet forms. Dry your hands before using this medication. This medication may come in a bottle or a blister pack.
- If using the blister pack, peel back the foil on the blister pack to remove a tablet.
- Do not push the tablet through the foil.
- Immediately after removing the tablet, place it on the tongue,
- Allow it to dissolve completely, then swallow it with saliva,
- You do not need to take this product with water.
- Doing so may increase your chance of getting a headache,
To prevent nausea from chemotherapy, take this medication usually within 30 minutes before treatment begins. To prevent nausea from radiation treatment, take this medication 1 to 2 hours before the start of your treatment. To prevent nausea after surgery, take ondansetron 1 hour before the start of surgery.
- This medication may be taken with or without food.
- However, your doctor may tell you not to eat before chemotherapy, radiation, or surgery.
- Take any other doses as directed by your doctor.
- Ondansetron may be taken up to 3 times a day for 1 to 2 days after your chemotherapy or radiation treatment is finished.
If you are taking this medication on a prescribed schedule, take it regularly in order to get the most benefit from it. To help you remember, take it at the same times each day. Dosage is based on your medical condition and response to therapy. The dosage for children may also be based on age and weight,
Can you eat or drink right after taking Zofran?
Zofran can be taken with or without food. Taking Zofran with a meal or snack may slightly enhance its effects, but eating may not be realistic if you’re already feeling nauseated. It’s also important to remember that your healthcare provider may tell you not to eat before certain cancer treatments or surgery.
Can you drink water while taking Zofran?
Use Ondansetron (Zofran) exactly as directed on the label, or as prescribed by your doctor. Do not use in larger or smaller amounts or for longer than recommended. Follow all directions on your prescription label. Do not take this medicine in larger or smaller amounts or for longer than recommended.
Keep the tablet in its blister pack until you are ready to take it. Open the package and peel back the foil. Do not push a tablet through the foil or you may damage the tablet.Use dry hands to remove the tablet and place it in your mouth.Do not swallow the tablet whole. Allow it to dissolve in your mouth without chewing.Swallow several times as the tablet dissolves.
To use ondansetron oral soluble film (strip) (Zuplenz):
Keep the strip in the foil pouch until you are ready to use the medicine.Using dry hands, remove the strip and place it on your tongue. It will begin to dissolve right away.Do not swallow the strip whole. Allow it to dissolve in your mouth without chewing.Swallow several times after the strip dissolves. If desired, you may drink liquid to help swallow the dissolved strip.Wash your hands after using Zuplenz.
Measure liquid medicine with the dosing syringe provided, or with a special dose-measuring spoon or medicine cup. If you do not have a dose-measuring device, ask your pharmacist for one. Store at room temperature away from moisture, heat, and light. Store liquid medicine in an upright position.
What not to do after taking Zofran?
5. Tips –
Take as directed. May be taken with or without food. When used to prevent nausea associated with chemotherapy, Zofran is usually taken 30 minutes before chemotherapy. When used to prevent nausea associated with radiotherapy, Zofran is usually taken one-to-two hours before radiotherapy. When used to prevent nausea associated with surgery, Zofran is usually taken one hour before anesthesia. The dose of Zofran orally disintegrating tablets is the same as Zofran solution. When taking the orally disintegrating tablets, peel back the foil (do not attempt to push the tablet through the foil). Allow the tablet to dissolve in your mouth without chewing. When taking Zofran oral solution, measure the correct dosage with the dosing syringe provided. Consider laxatives to relieve or prevent constipation associated with Zofran. Monitor for serotonin syndrome (symptoms include mental status changes ), fast heart rate, dizziness, flushing, muscle tremor or rigidity, and stomach symptoms ). Report to your doctor any other unusual side effects, such as a change in your heart rate, feeling lightheaded (especially when going from a sitting to a standing position), or if you develop any signs of an allergic reaction. If Zofran makes you dizzy or drowsy, do not drive or operate machinery while affected, and avoid alcohol. Tell your doctor or other health care provider about all the medicines you take, including prescription and over-the-counter (OTC) medicines, vitamins, and herbal supplements. Let them know if you eat grapefruit or drink grapefruit juice. Zofran interacts with several medicines and it may not be safe to take them together. Tell your doctor if you are pregnant or intend to become pregnant. It is not known how Zofran affects the unborn child. It is not known if Zofran is safe during breastfeeding.
What do I do if I throw up right after taking Zofran
Proper Use – Take this medicine only as directed by your doctor. Do not take more of it, do not take it more often, and do not take it for a longer time than your doctor ordered. This medicine comes with patient instructions. Read and follow these instructions carefully. Ask your doctor if you have any questions. To use the oral disintegrating tablet:
- Make sure your hands are dry.
- Do not push the tablet through the foil backing of the package. Instead, gently peel back the foil backing and remove the tablet.
- Immediately place the tablet on top of the tongue. The tablet will dissolve in seconds, and you may swallow it with your saliva. You do not need to drink water or other liquid to swallow the tablet.
To use the oral soluble film:
- Make sure your hands are clean and dry before and after using this medicine.
- Fold the pouch along the dotted line to expose the tear notch.
- While still folded, tear the pouch carefully along the edge and remove the film out from the pouch.
- Put the soluble film immediately on top of your tongue where it will dissolve in 4 to 20 seconds. Do not chew or swallow the film whole.
- Once the film is dissolved, you may swallow with or without water.
If you vomit within 30 minutes after using this medicine, take the same amount of medicine again. If vomiting continues, check with your doctor.
Will Zofran still work if you throw up after taking it?
If you vomit within one hour taking your first Zofran Tablet of each course prescribed to you, you should take the same dose again. If you continue to vomit, tell your doctor.
Can you give Zofran on an empty stomach?
To prevent nausea after surgery, take ondansetron by mouth 1 hour before the start of surgery. This medication may be taken with or without food. However, your doctor may tell you not to eat before chemotherapy, radiation, or surgery.
Does Zofran calm your stomach?
Zofran (ondansetron) prevents nausea and vomiting associated with chemotherapy and radiation. It’s also used to help with nausea and vomiting after surgery. Common side effects of Zofran are headache, fatigue, and stomach-related issues.
Will Zofran stop a stomach virus?
Zofran (ondansetron) can be used in emergency situations to treat severe vomiting and diarrhea in children with acute gastroenteritis (stomach flu). It’s also a drug commonly used to prevent severe nausea and vomiting in people undergoing cancer chemotherapy or radiation therapy.
Is it OK to drink water while nauseous?
Drink lots of fluids if possible, but start slowly with 1–2 sips every 5 minutes. If you become nauseated, wait 20–30 minutes and then begin again. Wait 20–30 minutes to be sure you don’t have more vomiting or diarrhea.
Does water help or worsen nausea
9 Foods That Help Relieve Nausea – A little fiber goes a long way toward clearing nausea-inducing chemicals out of your system, but too much at one time can make you feel even worse. “Fiber slows down digestion, so it’s possible that the slowing of the intestinal transit may help ease digestion and relieve nausea,” says Erin Palinski-Wade, RD, CDCES, author of Belly Fat Diet for Dummies,
But Palinski-Wade cautions that fiber may also do the opposite and trigger an increase in nausea. “I wouldn’t recommend high fiber foods as a cure for nausea in all circumstances,” she says. Throughout the day, snack sparingly on such fiber-rich foods as a whole apple (Gala apples are a good choice) and crunchy raw vegetables.
Try applesauce or apple juice if you’re having trouble digesting solid food. Foods high in starch — such as saltines, bread, and toast — help absorb gastric acid and settle a queasy stomach. “The bland nature of a cracker helps to satisfy hunger (excessive hunger can exacerbate nausea) without the strong smells or tastes that may increase nausea,” says Palinski-Wade. Capsules of powdered ginger have been found to reduce nausea and vomiting. You could also try a cup of ginger tea, a glass of ginger ale (some people swear it works better if it’s flat), a few gingersnap cookies, or a piece of ginger candy. “Ginger has been found to reduce symptoms of nausea, especially in pregnancy,” says Palinski-Wade. Small sips from a glass of plain water will help you stay hydrated — and avoid the headaches that often accompany nausea. Start out by slowly drinking tiny amounts until you feel you can stomach a larger amount. “Drinking fluids prevents hydration, but drinking too much at one time can make nausea worse,” says Palinski-Wade. A lack of protein can make nausea feel even worse, so look to protein-packed foods, such as nuts — even peanut butter, as long as you’re not allergic — that are easy to digest. They’ll quickly replenish your depleted energy and help keep your nausea at bay.
“Nausea from excessive hunger, low blood sugar, or pregnancy may respond well to the protein and fat in nuts,” says Palinski-Wade. But she cautions that if you’re fighting off a virus, nuts and protein may worsen nausea. “Typically a low-fat, lower protein meal plan that’s rich in starchy foods is the best solution when you’re struggling with nausea,” she says.
“Since protein and fat digests slowly, they may increase nausea in large amounts.” Chicken soup may make you feel better when you have a cold, but it’s too heavy when you’re nauseated. “Fats, which delay emptying of the stomach, should be avoided,” says Hanauer. Instead, try soothing your symptoms with chicken broth — the lower in fat, the better. Most sports drinks contain the electrolytes sodium and potassium, which help restore an athlete’s depleted nutrients. “Small sips of electrolyte-rich beverages are appropriate to promote hydration and replenish electrolytes lost during vomiting,” says Palinski-Wade. While you may not be up for sports, sports drinks can help even nonathletes feel better when they’re suffering from nausea. If your nausea is accompanied by dehydration, or if you have been vomiting, snack on a piece of this peel-and-eat fruit. Bananas can help restore potassium, which is often depleted as a result of diarrhea and vomiting. “Potassium is an electrolyte that’s lost during vomiting or bouts of diarrhea,” says Palinski-Wade. The refreshing aroma alone may be enough to make you feel better, but actually chewing on fresh mint or drinking a cup of mint tea is considered an effective remedy for nausea. “Deep breathing and other relaxation techniques may also be helpful,” says Hanauer.
Will Zofran make you sleepy?
Among the side effects from taking Zofran (ondansetron) are headaches, drowsiness, lightheadedness and constipation. In rare cases, the anti-nausea medication causes erratic heartbeats and potentially life-threatening high serotonin levels. By Jessica D. Hess, Ph.
Why am I throwing up after Zofran?
The mechanism of the drug involves blocking serotonin, which can cause vomiting. Doctors will look at your liver health and weight when deciding how much of the drug you should take. While Zofran can offer relief to some patients who can’t eat or struggle with chronic nausea, it can also create severe side effects.
How long after eating can I take Zofran
Popular FAQ – If you are taking ondansetron for nausea that occurs with meals, then the standard tablet should be taken half an hour to 1 hour before meals, and the orally disintegrating tablet or oral soluble film can be taken 15 minutes before meals.
However, if you are taking ondansetron for constant, all day nausea then it should be taken at regular intervals during the day as prescribed, with or without food. Oral ondansetron works quickly, usually within 30 minutes, but it can take up to two hours for the full effect. It’s taken before you receive medicines or procedures that might make you feel nauseous or cause vomiting.
Oral doses are usually taken 30 minutes before chemotherapy, 1 hour before surgery, or 1 to 2 hours before radiation treatments. You may need extra doses. Your doctor will tell you exactly when to take your medication. You can take ondansetron more frequently initially, for example, if you are taking it to prevent or treat nausea of vomiting from chemotherapy you can take 4mg then follow up with another 4mg dose at 4 and 8 hours after the first dose.
- The following day you should only take it every 8 hours (3 times a day).
- If you continue taking ondansetron more frequently than this you are at higher risk of side effects such as constipation, headache, or heart effects.
- Yes, ondansetron (Zofran) might make you feel sleepy or tired.
- Ondansetron injection for the treatment of post-operative nausea and vomiting has been reported to cause drowsiness or sedation in 8% of patients vs.7% of those using a placebo (an inactive treatment).
Malaise (generally feeling unwell) and fatigue (tiredness or lack of energy) have also been reported in 13% of patients (vs.2% placebo) when it is used orally for the prevention of chemotherapy-induced nausea and vomiting. Can you take ondansetron while pregnant? Although ondansetron is not specifically approved by the FDA to treat nausea and vomiting during pregnancy (NVP), its use is common, and approximately 25% of pregnant women are prescribed ondansetron to treat NVP.
Overall, studies show the use of ondansetron appears to be associated with an additional 3 instances of oral cleft defects (such as cleft lip or cleft palate) for every 10,000 women exposed to ondansetron during their first trimester. There may also be a very slight increased risk of a type of heart defect called a ventricular septal defect, but no apparent increased risk of other birth defects, miscarriage, or fetal death.
Ondansetron (Zofran) – Uses, Dosing, Side Effects
How many hours apart should you take Zofran?
Can you take Zofran every 6 hours? – The usual frequency of Zofran dosing in adults is an 8 mg tablet every 8-12 hours or 2-3 times a day. A scenario where you could take it more frequently would be if the dose taken was less than 8mg. Nevertheless, the sum of the doses taken cannot exceed 8 mg within that time frame.
What if Zofran is not working for nausea?
If your nausea does not ease by 30 minutes after taking Zofran, take medicine #2, prochlorperazine (Compazine).
Does Zofran help with anxiety?
Behavioural pharmacologyOndansetron, a 5HT3 receptor antagonist reverses depression and anxiety-like behavior in streptozotocin-induced diabetic mice: Possible implication of serotonergic system , 5 December 2014, Pages 59-66 Mood disorders such as depression and anxiety comorbid with diabetes are emerging problems that warrant immediate research attention. It has been reported that diabetic patients are almost twice as likely to have depression and anxiety as non-diabetic individuals that point to a third of diabetic population (Anderson et al., 2001, Egede et al., 2002, Furuya et al., 2013, Grant et al., 2013, Lustman and Clouse, 2005, Trento et al., 2012).
Depression and anxiety comorbid with diabetes not only worse quality of life but also glycemic control (an increased risk for the development of diabetes complications) and increase morbidity and mortality rates (Ciechanowski et al., 2000, Gary et al., 2000, Huang et al., 2011). Screening neurobehavioral consequences such as depression and anxiety in preclinical diabetic model can help to elucidate the pathophysiology of this comorbidity and to identify the specific targets for therapy.
Streptozotocin (STZ) is an agent of choice to induce diabetes in animals. It inhibits insulin secretion by specific necrosis of pancreatic beta cells resulting insulin dependent diabetes (Lenzen, 2008). Previous reports have shown that STZ-induced diabetes results in several depression and anxiety-like behavioral deficits in rodents.
STZ-induced diabetes has demonstrated increased duration of immobility in behavioral despair tests of depression like forced swim test (FST) and tail suspension test (TST) (Hirano et al., 2007, Kamei et al., 2003, Miyata et al., 2004). In addition, STZ-induced diabetes has shown to elicit anxiety-like behavioral deficits in rodents subjected to social interaction and zero maze tests (Ramanathan et al., 1998).
STZ-induced diabetes has demonstrated increased time spent in closed arms in elevated plus maze (EPM) and reduced time spent in central arena in open field test (Aksu et al., 2012), the behavioral models of anxiety. Thus, STZ-induced diabetes is a suitable model to study diabetes induced behavioral effects and to evaluate clinical potential of compounds for treating mood disorders comorbid with diabetes.
Several attempts have been made to mitigate depression and anxiety-like behavioral consequences of diabetes. Clinical studies have evidenced the efficacy of currently existing antidepressants such as fluoxetine and citalopram (selective serotonin reuptake inhibitors, SSRIs) to attenuate these disorders comorbid with diabetes (Goodnick, 2001, Lustman et al., 2000, Petrak and Herpertz, 2009).
The effectiveness of these drugs is based on the correction of altered monoaminergic functions in the brain (Goodnick, 2001). Monoamine, serotonin is among the key neurotransmitters, which regulate behavior and emotional activities in the brain. The well-coordinated activation and inhibition of this neurotransmitter system in normal brain has shown to be disrupted in diabetes (Shpakov et al., 2011).
In particular, diabetes patients have reported a significant decrease in serotonin levels in the brain with persistent depressive behavior and altered mood functions, which has shown to be normalized by chronic treatment with antidepressants (Manjarrez-Gutierrez et al., 2009; for review see: Ho et al., 2013, Shpakov et al., 2011).
Similarly, preclinical studies have revealed that STZ-induced diabetic rodents exhibit reduced serotonin levels in the brain (Miyata et al., 2007, Sandrini et al., 1997, Chu et al., 1986). On the other hand, repeated administration of antidepressants (such as fluoxetine) results in significant increase in brain content of serotonin in diabetic rodents (Kolta et al., 1986).
Altogether, these findings suggest that diabetes may lead to a significant decreased activity of serotonin that may account for depression and anxiety-like comorbid behavioral deficits and reversal of distressed activity of the neurotransmitter may ameliorate the behavioral consequences of chronic diabetic state.
Although, currently existing antidepressants result in recovery of depression and anxiety, there exist a number of limitations such as delayed onset of therapeutic effects, low remission rates, drug interactions, and frequent and persistent side effects (Gumnick and Nemeroff, 2000, Masand, 2003, Robinson, 2003).
Moreover, comorbidity with diabetes has shown to worsen the response of antidepressant interventions while, conventional antidepressants have been found to impair glycemic control and hence increase risk of complications in diabetes patients (de Groot et al., 2001, Lustman et al., 1988, Musselman et al., 2003).
Preclinical investigations have demonstrated that diabetes attenuates antidepressant effects of drugs like fluoxetine, chlomipramine and imipramine in rodents (Li and France, 2008, Massol et al., 1989, Miyata et al., 2004). Lustman et al. (1997) have shown that nortriptyline, a tricyclic antidepressant worse glycemic control in diabetes patients.
Acute central administration of fluoxetine induces hyperglycemia in mice (Carvalho et al., 2004). Treatment with imipramine results in increased body mass index and decreased insulin secretion in depressed patients (Moosa et al., 2003). Repeated administration of mirtazapine is associated with increased body weight, body fat mass and leptin concentration (Laimer et al., 2006).
It suggests that there are critical unmet needs for new drugs which exert a potential antidepressant effects and overcome the drawbacks of existing antidepressant pharmacotherapy for treatment of depression and anxiety-like disorders comorbid with diabetes.
- Ondansetron is a selective 5HT 3 receptor antagonist, which has shown potential antidepressant and anxiolytic effects in neuro-psychopharmacological investigations.
- Preclinical studies have evidenced that it reduces duration of immobility in mouse FST and TST (Ramamoorthy et al., 2008).
- In addition, ondansetron has shown modified behavior in elevated plus maze, light–dark box and other anxiolytic testing paradigms, substantially demonstrating the anti-anxiety activity (Bourin and Hascoet, 2003, Rodgers et al., 1997, Roychoudhury and Kulkarni, 1997).
Pretreatment of ondansetron has reported to potentiate antidepressant effects of several antidepressants (Redrobe and Bourin, 1997). On the other hand, chronic treatment with ondansetron has shown to reverse depression and anxiety-like behavior in olfactory bulbectomized rats (Ramamoorthy et al., 2008).
In our recent study, we have reported that ondansetron treatment reverses chronic stress-induced depression-like behavior in mice (Gupta et al., 2014a). Evidences from clinical studies have revealed a significant antidepressant activity of the drug in comorbid conditions such as depression associated with early onset alcoholics (Johnson et al., 2003), obsessive compulsive disorder (Hewlett et al., 2003), chronic hepatitis C-infected (Piche et al., 2005) and bulimia nervosa patients (Faris et al., 2006).
In some of the clinical trials, ondansetron has been reported as effective in controlling anxiety. Harmer et al. (2006) have shown that ondansetron abolishes emotions induced startle effects in humans. Interestingly, the therapeutic effect of the drug (in addition to several 5HT 3 receptor antagonists) has been reported to occur at low dose ranges and improvement in depression and anxiety-related symptoms have been evident within 2–3 weeks of administration (Faris et al., 2006, Hewlett et al., 2003, Piche et al., 2005).
- This suggest the potential activity of ondansetron in alleviating depression and anxiety, however, the effects of the drug in diabetes conditions are still remain to be determined.
- Therefore, the aim of the present study was (i) to examine the effects of ondansetron in reversing depression and anxiety-like behavior in streptozotocin-induced diabetic mice, and (ii) to elucidate the possible implication of serotonergic neurotransmitter system in mediating the antidepressant-like activity of ondansetron in rodent depressive states comorbid with diabetes.
Swiss Albino male mice (22–25 g) were obtained from Hisar Agricultural University, Haryana, India. Animals were group housed in cages and were maintained in standard laboratory conditions with alternating light–dark cycle of 12 h each, temperature 23±2 ° C and humidity conditions 62±5% relative humidity in the housing unit.
Animals had free access to standard pellet chow feed (except during estimation of fasted blood glucose levels, where mice were fasted overnight) and filtered water ad libitum. While assessing the behavioral activity on the basis of duration of immobility or the exploratory behavior of rodents, the effect of general increase in the locomotor activity may possibly give false positive results.
Therefore, the basal locomotor activity was assessed to determine the effect of persistent diabetic state and drug treatment (ondansetron, 0.5 and 1 mg/kg and fluoxetine, 10 mg/kg) on generalized increase in locomotor scores. The results showed that, STZ-induced diabetes had no The present study demonstrates for the first time that ondansetron, a 5HT 3 receptor antagonist is effective in ameliorating depression and anxiety-like behavior associated with diabetes in streptozotocin-induced diabetic mice.
I. Aksu et al. F. Borsini M. Bourin et al. J.M. Brezun et al. A. Bystritsky et al. F. Carvalho et al. J.F. Cryan et al. A. Dranovsky et al. P.L. Faris et al. P. Grant et al.
D. Gupta et al. M. Hascoet et al. S. Hirano et al. N. Ho et al. C.J. Huang et al. J. Kamei et al. P.J. Lustman et al. H. Manev et al. P.S. Masand J. Massol et al. S. Miyata et al. D.L. Musselman et al. A. Ramos J.P. Redrobe et al. R.J. Rodgers et al. M. Sandrini et al. H. Takeda et al.
Diabetic encephalopathy is related to serious damage to the Central Nervous System leading to several disturbances in memory processing and emotions. It is known that the cyclic adenosine 3′,5′-monophosphate (cAMP) responsive element-binding protein (CREB) pathway participates in neuronal plasticity and prevention of neuroinflammation, as well as the mediation of learning/memory processes and emotions in brain areas such as the hippocampus (HIP) and prefrontal cortex (PFC). We aimed to investigate the effect of acute (one injection) and long-term treatment (21 days) with roflumilast (ROF; i.p.; 0, 0.01, 0.03, 0.1 mg/kg), a drug able to inhibit the enzyme phosphodiesterase-4 (PDE-4) responsible for cAMP hydrolysis, on parameters related to the acquisition of fear extinction memory and anxiety-like responses in animals with type-1 diabetes mellitus (T1DM) induced through one injection of streptozotocin (60 mg/kg; ip; STZ animals). When we performed acute treatment, no difference was observed between all the groups when resubmitted to the same context paired with an aversive stimulus (footshock) or to a neutral context. In contrast, long-term treatment was able to improve learning of extinction fear memory and discriminating between a conditioned and neutral context. Moreover, this treatment decreased the pronounced anxiety-like response of STZ animals. In addition, there was an increase in the product of the CREB signaling pathway, the pro brain-derived neurotrophic factor, in the HIP and PFC of these animals. The treatment did not impair glycemic control, whereas it decreased the animal’s blood glucose levels. To conclude, these findings suggest that ROF treatment repositioning has potential for future translational investigations involving diabetic patients considering its beneficial effects on emotional processes related to fear memory and anxiety, in addition to improvement of glycemic control. Mirtazapine, an atypical antidepressant, is known to enhance serotonergic transmission by inhibiting the 5-hydroxytryptamine (5-HT) 1A, 5-HT 2C, and 5-HT 3 receptors. However, the mechanism of action on the 5-HT 3 receptor remains unclear. We investigated the inhibitory mechanisms of mirtazapine on 5-HT 3 receptors of NCB20 neuroblastoma cells using the whole-cell voltage-clamp method. Mirtazapine inhibited the 5-HT 3 receptor currents in a concentration-dependent manner, and the inhibitory effect was influenced by the concentration of 5-HT. When mirtazapine was co-applied to 5-HT, the maximal response of the 5-HT 3 receptor current was reduced and EC 50 was increased, suggesting that mirtazapine might act as a non-competitive inhibitor. Inhibition of 5-HT 3 current by mirtazapine was stronger in pre-application than in co-application, which suggests that mirtazapine might act as a closed state inhibitor. This finding was further supported by no use-dependency of the mirtazapine for 5-HT 3 receptor inhibition. Finally, mirtazapine accelerated the desensitization and deactivation process in a concentration-dependent manner. The difference in recovery time showed that mirtazapine drastically influences the desensitization process than the deactivation process. These mechanistic characteristics of mirtazapine support the understanding of the relationship between the 5-HT 3 receptor and atypical antidepressants. Treating depression associated with type-1 diabetes mellitus (T1DM) is a major clinical challenge. Fish oil (FO), composed mostly of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), has been pointed out as quite promising for the treatment of depression given its neuroprotective property. Although DHA and EPA exert several physiological actions, DHA is known to play a critical role in postnatal brain development. This study aimed to investigate the effect of preventive treatment with FO (with more DHA in the composition) alone or associated with antidepressant drugs on depression-like behaviors and brain monoamines levels of juvenile induced-T1DM rats. Thus, prepubescent rats were submitted to a prolonged treatment with vehicle (VEH) or FO (50% of DHA and 20% EPA) starting 4 weeks before the induction of experimental T1DM (on day 28) by streptozotocin. When combined, the treatment with vehicle, fluoxetine (FLX, a selective serotonin reuptake inhibitor) or imipramine (IMI, a tricyclic antidepressant) started at week 6 (day 42) and lasted for 2 weeks (until day 56). The behavioral tests were conducted on days 55 and 56, followed by hippocampal and prefrontal cortex dissection for neurochemical analyses. Our results showed that induced-T1DM rats pretreated with FO showed a significant increase of EPA and DHA in plasma, indicative of an increase in the systemic availability of these acids. As previously observed, induced-T1DM rats presented increased immobility and decreased swimming and climbing frequencies in the modified forced swimming test, indicative of depressive-like behavior. Only the combined treatment – FO plus antidepressants (FLX or IMI – both in the highest dose) – was able to induce a significant improvement of depressive-like behaviors. Here, it is noteworthy that swimming behavior has been associated with an increase in serotonergic neurotransmission. Interestingly, our data showed that the combined treatment (FO + antidepressants – including the ineffective dose of FLX) was able to increase the swimming of animals more significantly compared to animals not pretreated with FO. In addition, confirming these assumptions, the decreased 5-HT levels in the hippocampus from induced-T1DM rats were increased after treatment with FLX (highest dose) or IMI (both doses), being this increase more pronounced in animal pretreated with FO. Intriguingly, in these animals pretreated with FO, the ineffective dose of FLX in association with FO was able to increase the levels of 5-HT. The decreased hippocampal levels of noradrenaline were increased only after IMI treatment, not being influenced by FO pretreatment. In conclusion, ours results pointed out that the choice of the DHA/EPA ratio may be an important factor to be considered for the FO antidepressant-like effect per se, but the FO treatment in this composition associated with the antidepressant drugs – especially that ones that increase preferentially the availability of 5-HT -, may represent a better alternative of treatment to individuals with T1DM-associated depression. The prevalence rates of depression and anxiety are at least two times higher in diabetic patients, increasing morbidity and mortality. Cannabidiol (CBD) has been identified as a therapeutic agent viable to treat diverse psychiatric disorders. Thus, this study aimed to investigate the effect of CBD treatment (once a day for 14 days starting two weeks after diabetes induction; at doses of 0, 3, 10 or 30 mg/kg, i.p.) on depression- and anxiety-like behaviors associated with experimental diabetes induced by streptozotocin (60 mg/kg; i.p.) in rats. Levels of plasma insulin, blood glucose, and weight gain were evaluated in all experimental groups, including a positive control group treated with imipramine. The rats were tested in the modified forced swimming test (mFST) and elevated plus maze (EPM) test. Besides, the levels of serotonin (5-HT), noradrenaline (NA) and dopamine (DA) in two emotion-related brain regions, the prefrontal cortex (PFC) and hippocampus (HIP) were evaluated using high-pressure liquid chromatography. Our results showed that CBD treatment (only at the higher dose of 30 mg/kg) reduced the exaggerated depressive- and anxiogenic-like behaviors of diabetic (DBT) rats, which may be associated with altered 5-HT, NA and/or DA levels observed in the PFC and HIP. Treatment with CBD (higher dose) also induced a significant increase in weight gain and the insulin levels (and consequently reduced glycemia) in DBT rats. The long-term CBD effects gave rise to novel therapeutic strategies to limit the physiological and neurobehavioral deficits in DBT rats. This approach provided evidence that CBD can be useful for treating psychiatry comorbidities in diabetic patients. Diabetes is a metabolic disease characterized by hyperglycemia because of insulin resistance and/or insufficient insulin release. The most common diabetic brain complications include cognitive decline and depression. The present study investigated whether the 4–4′-dichlorodiphenyl diselenide ( p -ClPhSe) 2 is effective against memory impairment induced by diabetes in mice and the role of hippocampal BDNF/TrkB signaling in this effect. Male adult Swiss mice received an injection of streptozotocin (STZ) (200 mg/kg, i.p.) to induce diabetes. The results revealed that STZ injection in mice resulted in resilience (glycemia <200 mg/dl) or diabetes (glycemia ≥200 mg/dl). The vehicle-control group received citrate buffer (5 ml/kg). The animals were subchronically treated with ( p -ClPhSe) 2 (1 or 5 mg/kg, i.g.) for 7 days. Mice performed a battery of well-validated behavior tests designated to evaluate memory, object recognition (ORT), object location (OLT), and Morris water maze (MWM). The hippocampal protein contents of the BDNF/TrkB pathway were determined in the samples of experimental groups. Fluoro Jade C (FJC) was used for staining degenerating neurons. The STZ administration resulted in memory impairment that was demonstrated in the mouse ORT, OLT, and MWM tests. The molecular findings indicate an increase in hippocampal protein levels of proBDNF and TrKB but a decrease in those of mBDNF and pCREB in diabetic mice. The number of FJC-positive cells was increased in the hippocampus of diabetic mice. ( p -ClPhSe) 2 at the dose of 5 mg/kg modulated the hippocampal BDNF/TrkB pathway, reduced FJC-positive cells and reversed memory impairment induced by STZ in mice. These findings demonstrate the effectiveness of ( p -ClPhSe) 2 against memory impairment caused by diabetes in mice. ( p -ClPhSe) 2 modulated the hippocampal BDNF/TrkB signaling pathway in diabetic mice. Diabetes mellitus (DM) is a common metabolic disorder that affects multiple organ systems. DM also affects brain processes, contributing to various CNS disorders, including depression, anxiety and Alzheimer's disease. Despite active research in humans, rodent models and in-vitro systems, the pathogenetic link between DM and brain disorders remains poorly understood. Novel translational models and new model organisms are therefore essential to more fully study the impact of DM on CNS. The zebrafish ( Danio rerio ) is a powerful novel model species to study metabolic and CNS disorders. Here, we discuss how DM alters brain functions and behavior in zebrafish, and summarize their translational relevance to studying DM-related CNS pathogenesis in humans. We recognize the growing utility of zebrafish models in translational DM research, as they continue to improve our understanding of different brain pathologies associated with DM, and may foster the discovery of drugs that prevent or treat these diseases.
The major aim of this multicenter study of the European Group for the Study of Resistant Depression (GSRD) was to elucidate associations between major depressive disorder (MDD) and comorbid diabetes. Demographic and clinical information of 1410 patients with a primary MDD diagnosis according to DSM-IV were retrieved cross-sectionally between 2012 and 2016. By applying descriptive statistics, analyses of covariance (ANCOVA) and binary logistic regression analyses, a comparison between patient characteristics with and without comorbid diabetes was performed. The point prevalence rate for comorbid diabetes across MDD patients was 6%. Individuals with MDD + comorbid diabetes were significantly older, heavier, more likely to be inpatient and diagnosed with additional comorbid chronic somatic diseases. In addition, current suicide risk was significantly increased and melancholic features were more likely pronounced. In general, patients in the MDD + diabetes group received a combination therapy with at least one additional antidepressant rather than various other augmentation strategies. Our analyses depict a lower prevalence rate of diabetes in MDD patients than previous studies. However, in light of the prevalence of diabetes in the geographical area of the study, we found an increased risk for individuals with depression compared to the general population. Current suicide risk is markedly elevated and has to be thoroughly assessed in every patient with comorbid diabetes. Depression severity and treatment response remained unaffected by concurrent diabetes in MDD. Object : The aim of this study was to evaluate low-dose ondansetron as an augmentation strategy in patients with obsessive-compulsive disorder (OCD) who do not adequately respond to serotonin reuptake inhibits (SRIs). Methods : Twenty-one OCD patients who had not responded adequately to an SRI received 12 weeks of single-blind ondansetron augmentation initiated at 0.25 mg BID for 2 weeks, and titrated to 0.5 mg BID for an additional 10 weeks. Patients were rated every two weeks using the Yale–Brown Obsessive Compulsive Scale (YBOCS) and Clinical Global Impressions Scale (CGI). Treatment response was defined as an additional 25% reduction in YBOCS score from the score at the initiation of ondansetron augmentation, an end of treatment YBOCS score of ≤24 and a CGI-Improvement (CGI-I) score of ≤2. Upon completion of treatment course patients were followed for 4 weeks. Results : At week 12, twelve of the 21 (57%) patients were responders. The average reduction in the YBOCS score for the overall group was 27.2%. Responders had an average 44% YBOCS score reduction and 76.9% CGI-I reduction. After discontinuation of ondansetron the YBOCS worsened an average of 15.5% in the entire sample and 38.3% in the responder subsample. No clinically meaningful side effects were reported. Conclusion : OCD patients who do not adequately respond to an SRI may benefit from augmentation with a low-dose of ondansetron. This may provide an alternative approach to augmentation with atypical antipsychotic agents, with a more favorable safety profile. Pioglitazone is a member of peroxisome proliferator-activated receptor gamma (PPARγ) agonists, particularly used in management of type II diabetes. However it also has effects in some dermatological disorders. The current study was designed to investigate the effects of oral administration of pioglitazone and the association of nitric oxide, in serotonin-induced scratching in mice. In order to produce the scratching activity, serotonin (141 nm/site) was administered intradermally in the nape of the neck. Pioglitazone in concentrations of 10, 20, 40 and 80 mg/kg, was peroral administered (p.o) as a single dose, 4 h before the serotonin injection. PPAR-γ antagonist, GW9662 (2 mg/kg, i.p); a non-specific nitric oxide synthase (NOS) inhibitor, NG-nitro- l -arginine methyl ester ( l -NAME; 1 mg/kg, i.p); or a nitric oxide precursor, l -arginine (100 mg/kg, i.p.); adminstrated 15 min before pioglitazone were analyzed for anti-scratching activity. Results obtained showed that pioglitazone (40 and 80 mg/kg, p.o) reduced the scratching in a dose-dependent manner. GW9662 inverted the anti-scratching effect of pioglitazone (80 mg/kg). Acute dose of l -NAME (1 mg/kg, i.p) also prevented the anti-scratching property of pioglitazone (80 mg/kg, p.o); although l -arginine was used in sub-effective dose (100 mg/kg, i.p), however it potentiated the anti-scratching behavior when co-injected with pioglitazone (20 mg/kg, p.o). The results indicate that acute pioglitazone has an anti-scratching effect on serotonin-induced scratching in mice. It is concluded that anti-scratching outcome of acute pioglitazone is initiated via activation of PPAR-γ receptor and to some extent by the NO pathway. Diabetes Mellitus (DM) and depression occur comorbidly and share some pathophysiological mechanisms. The course of depression in patients with the two conditions is severe. Treatment of depression in diabetic patients requires special attention because most of psychopharmacological agents can worsen glycemic control. This article aims to review studies evaluating the antidepressant effect of anti-hyperglycemic agents from preclinical perspective. A literature search was performed with PubMed and Google Scholar using relevant keywords (antidiabetic; diabetes; depression; antidepressant; animals) to extract relevant studies evaluating the antidepressant activity of anti-hyperglycemic agents in experimental models. Several studies have reported that some traditional anti-hyperglycemic agents reduce depression-like behavior in the absence or presence of diabetes. These drugs include insulin, glyburide, metformin, pioglitazone, vildagliptin, liraglutide, and exenatide. The antidepressant activity of anti-hyperglycemic agents may be mediated by reducing the blood glucose level, ameliorating the central oxidative stress and inflammation, and regulating the hypothalamic–pituitary–adrenal axis (HPAA). Drugs which have both antidiabetic and antidepressant activities can provide better treatment strategy for patients with diabetes-associated depression. However, further research studies are still required in human subjects. Studies showing anxiolytic-like properties of natural products have grown. This paper evaluated if carvacryl acetate (CA) could be studied as an alternative drug to treat anxiety disorders. Elevated plus maze (EPM) tests, light-dark box (LDB) tests, and marble-burying tests (MBTs) were performed on mice. In the first protocol, the anxiolytic-like activities of CA 25, 50, 75 and 100 mg/kg at single doses were compared to those of the vehicle, buspirone 5 mg/kg (BUSP) and diazepam 1 mg/kg (DZP). In the second protocol, the anxiolytic-like actions of CA were tested for GABAergic and serotonergic systems. The time spent in the open arms (TSOA) and the number of open arms entries (NOAE) were measured in EPM; the time spent in the light box (TSLB) and the number of entries to light box (NELB) were measured in LDB; and the number of marbles buried (NMB) were measured in MBT. CA increased TSOA and NOAE in the EPM, as well as TSLB and NELB in the LDB and the NMB in the MBT. The anxiolytic-like activity of CA 25; 50; 75 and 100 mg/kg was not associated with psychomotor retardation in the open field test and in the Rota rod test, contrarily with what happened with DZP. In the second protocol, to suggest the mechanism of action of CA, flumazenil 25 mg/kg ip (FLU) and WAY 100,635 10 mg/kg ip (WAY–5-HT1A antagonist) were also used. FLU + CA100 reduced TSOA in the EPM when compared to CA100 but WAY + CA100 did not. In LDB, FLU + CA100 reduced the TSLB when compared to CA100 but WAY + CA100 did not. In the MBT, FLU + CA100 inhibited the effect of CA100 on the NMB but WAY + CA100 did not. In conclusion, CA seems to have an anxiolytic-like effect, probably due to GABAergic agonist action, without psychomotor side effects. Although the pathophysiology of major depression disorder (MDD) is still poorly understood, mounting evidence suggests that the brains of depressed patients are under oxidative stress, leading to depressive symptoms that may include anxiety and cognitive impairment. This study aimed to investigate if the seleno-organic compound 1-methyl-3-(phenylselanyl)-1H-indole (MFSeI) reverses the depression- and anxiogenic-like behaviour, cognitive impairment and oxidative stress induced by the intra-cerebroventricular injection of streptozotocin (STZ; 0.2 mg/4 μl/per mouse) in Swiss male mice. Twenty-four hours after the STZ injection, mice were treated with MFSeI (10 mg/kg, intra-gastrically), or vehicle solution, once daily for seven days. The behavioural tests were performed 30 min after the final MFSeI administration, followed by euthanasia and collection of the cerebral cortex and hippocampus. Administration of MFSeI reversed the depression- and anxiogenic-like behaviour and cognitive impairment induced by STZ, in mice. Neurochemical analyses demonstrated that MFSeI reversed the STZ-increased levels of reactive species, nitrite, lipid peroxidation and acetylcholinesterase activity in the cerebral cortex and hippocampus of mice. Moreover, a single administration of MFSeI (300 mg/kg, intra-gastrically) did not cause acute toxicity in Swiss male mice. Altogether, our data suggest that MFSeI exhibits antidepressant- and anxiolytic-like effects and improves the cognition of STZ-treated mice, without any toxicity.
: Behavioural pharmacologyOndansetron, a 5HT3 receptor antagonist reverses depression and anxiety-like behavior in streptozotocin-induced diabetic mice: Possible implication of serotonergic system
How long does it take for Zofran to be absorbed?
Mechanism of Action – Ondansetron is a selective 5-HT3 serotonin-receptor antagonist used for its antiemetic properties. It is one of the four FDA-approved 5-HT3 serotonin-receptor antagonists used to combat nausea and vomiting, including granisetron, dolasetron, and the second-generation drug, palonosetron.
Ondansetron acts both centrally and peripherally to prevent and treat nausea and vomiting. Central effects are mediated by the antagonism of 5HT-3 serotonin receptors in the area postrema. The area postrema, located on the fourth ventricle floor, contains the “chemoreceptor trigger zone.” This zone senses neurotransmitters like serotonin, toxins, and other signals and plays a role in mediating the sensation of nausea and subsequent vomiting.
Ondansetron also has effects peripherally by acting on the vagus nerve. It works on the 5-HT3 receptors that can be found at the vagus nerve terminals. The vagus nerve can sense nausea and vomiting triggers within the GI tract, such as stomach irritants.
It forms synapses within the nucleus tractus solitarius of the brainstem, another region important in vomiting. The peripheral actions of ondansetron are thought to be the predominant mechanism for its antiemetic effects. Pharmacokinetics Absorption: Ondansetron undergoes rapid absorption from the GI tract, and the peak plasma concentration (Tmax) is approximately 1.5 hours after an 8 mg single oral dose.
The absolute bioavailability of ondansetron after oral administration is approximately 60%(50%-70%). The lower bioavailability is attributed to first-pass metabolism. The systemic bioavailability of ondansetron increases nonlinearly with increasing doses from 8 mg, 16 mg, 32 mg, and 64 mg because of saturation of the first-pass metabolism.
The bioavailability of ondansetron is significantly higher in patients with cancer (85% to 87%) than in healthy individuals (50%-70%), possibly due to alterations in metabolism. Distribution : Ondansetron and its metabolites are extensively distributed in tissues. The apparent volume of distribution(Vd) at a steady state is approximately 1.8 L/kg.
Ondansetron crosses the blood-brain barrier to a lower extent, with the CSF concentration only about 10%-15% of the plasma concentration in human volunteers. Adenosine binding cassette subfamily 1(ABCB1) is a drug efflux transporter known to transport ondansetron across the blood-brain barrier, thus limiting its accumulation in the CNS.
In a patient with decreased activity of ABCB1, the concentration of ondansetron in the brain increases and improves efficacy. Metabolism: The liver is the primary site of metabolism. The primary mechanism of metabolism is oxidation.8-hydroxy ondansetron represents the major metabolite (40%), followed by 7-hydroxy ondansetron ( Excretion: Hepatic metabolism accounts for nearly 95% of ondansetron clearance, and less than 5% is excreted unchanged in the urine.
The clearance and elimination half-life of ondansetron vary according to age. The elimination half-life after an 8 mg oral or intravenous dose is approximately 3-4 h in adults, but on average, it is 5.5 hours in the elderly. Clearance ranges from 0.381 L/h/kg to 0.262 L/h/kg, depending on age.
Can you drink after taking anti nausea medicine
Anti-Nausea Medications – Medications that are prescribed to treat nausea can make you feel drowsy, dizzy, and may impair your motor control—symptoms that can also be caused by alcohol. Some drugs (often antihistamines) used to prevent and treat motion sickness can also be purchased over-the-counter.
Antivert (meclizine)Atarax (hydroxyzine)Phenergan (promethazine)
Certain types of anti-nausea medication can be used to help someone who is trying to stop drinking alcohol. When used under medical supervision, the combination can be an effective way to treat alcohol withdrawal.
How many hours apart should you take Zofran?
Can you take Zofran every 6 hours? – The usual frequency of Zofran dosing in adults is an 8 mg tablet every 8-12 hours or 2-3 times a day. A scenario where you could take it more frequently would be if the dose taken was less than 8mg. Nevertheless, the sum of the doses taken cannot exceed 8 mg within that time frame.
Why do I still feel sick after taking Zofran
Common Zofran Side Effects – Zofran (ondansetron) is used to relieve nausea and vomiting regularly associated with cancer treatments such as chemotherapy and radiation. Doctors can also use it to prevent and treat post-surgical nausea and vomiting. Providers often prescribe Zofran for nausea associated with pregnancy and morning sickness, but this is an off-label, or unapproved, use of the drug.
Headache Constipation Chills Drowsiness Tiredness Weakness
These side effects are not serious unless they linger more than a few days. Zofran can also mask signs of a bowel obstruction in people who have just had abdominal surgery or those going through chemotherapy or radiation therapy. Even common side effects from the drug are rare, but you may feel sick to your stomach after taking Zofran.