Generic Zofran is used for preventing nausea and vomiting due to cancer chemotherapy or surgery. It may also be used for other conditions.
Other names for this medication:
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Also known as: Ondansetron.
Generic Zofran is used for preventing nausea and vomiting due to cancer chemotherapy or surgery. It may also be used for other conditions.
Generic Zofran is a serotonin 5-HT3 receptor blocker. It works by blocking a chemical thought to be a cause of nausea and vomiting in certain situations (e.g., chemotherapy).
Zofran is also known as Ondansetron, Vomiof, Danzetron, Ondaz.
Generic name of Generic Zofran is Ondansetron.
Brand name of Generic Zofran is Zofran.
Take each dose with a full glass of water.
Take Generic Zofran with food or an antacid to lessen stomach discomfort.
If you want to achieve most effective results do not stop taking Generic Zofran suddenly.
If you overdose Generic Zofran and you don't feel good you should visit your doctor or health care provider immediately.
Store at temperature between 2 and 30 degrees C (36 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Zofran are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Generic Zofran if you are allergic to Generic Zofran components.
Be careful with Generic Zofran if you're pregnant or you plan to have a baby, or you are a nursing mother.
Generic Zofran should be used with extreme caution in children younger than 4 months old. Safety and effectiveness in these children have not been confirmed.
Do not stop taking Generic Zofran suddenly.
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A novel series of benzamides with a hexahydro-1,4-diazepine or hexahydroazepine ring in the amine moiety were prepared, and their binding affinities for 5-HT3 and dopamine D2 receptors were evaluated. The R isomer of the 1-ethyl-4-methylhexahydro-1,4-diazepinylbenzamide (R)-22 had potent affinity for both receptors. The R-enantiomer of the corresponding 1-ethylhexahydroazepinylbenzamide 28 showed potent affinity for dopamine D2 receptors with reduced affinity for 5-HT3 receptors, while the S isomer was found to be a potent and selective 5-HT3 receptor antagonist.
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The pathogenesis of initiating the pruritus in patients with cholestasis is still not completely understood. One hypothesis is, that the cause for initiating the pruritus in patients with cholestasis is the activation of nerves in the skin. The activating substances are unknown, probably they are substances who accumulate in patients with cholestasis. Therefore one of the conventional approaches to treat pruritus is to remove pruritogenic substances from the body. Examples of this approach include the administration of anion exchange resins as cholestyramine or the administration of hepatic enzyme-inducing drugs such as rifampicin or phenobarbital. None of these drugs has been conclusively shown to be efficacious. A new hypothesis is the association of pruritus with altered central neurotransmission. Altered opioid concentrations probably play a central role in the pathogenesis of pruritus. This hypothesis is corroborate by the possibility of treating pruritus in patients with cholestasis with opiate antagonists such as naloxone or nalmefene. The treatment with ondansetron may also have effects on the pruritus of patients with cholestasis. A completely new treatment strategy is the application of dronabinol (r-9-tetrahydrocannabinol).
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In 51 450 patient visits (24 834 preintervention, 26 616 postintervention) seen by 96 physicians, we observed reduced postintervention use of abdominal and pelvic and head computed tomography scans, chest radiographs, intravenous antibiotics, and ondansetron (P < .01 for all). Hospital admissions decreased from 7.4% to 6.7% (P = .002), length of stay from 112 to 108 minutes (P < .001), and RR from 2.2% to 2.0%. Trends for use of laboratory tests and intravenous antibiotics showed significant reduction (P < .001 and P < .05, respectively); admission trends increased, and trends for use of computed tomography scans and plain abdominal radiographs showed no change.
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Ondansetron, a selective serotonin type 3 receptor antagonist, has been investigated at a wide range of doses. Recent studies have demonstrated that a single dose of this drug is active, either by intravenous bolus or continuous infusion. The main aim of this study was to evaluate the efficacy of a low dose of ondansetron in a simple and feasible schedule as follows: ondansetron 8 mg i.v. and dexamethasone 8 mg i.v. given before chemotherapy on day 1. Oral ondansetron 8 mg was subsequently given in the evening of day 1, and then even 12 hours on days 2, 3 and 4.
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There was a highly significant improvement in P50 gating after ondansetron treatment. The maximal treatment difference was at 2 hours posttreatment (ondansetron: mean=41.4%, SD=39.7%; placebo: mean=80.2%, SD=21.3%).
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A retrospective review of the senior author's experience over 5 years (1998 to 2004) of ambulatory alveolar cleft closure was compared with the previous 5-year period (1993 to 1998) of inpatient convalescence. An iliac crest donor site and standard techniques of alveolar grafting were followed in both groups. Although local analgesia with lidocaine and epinephrine was used in both groups, the ambulatory group received preemptive local anesthesia augmented with Marcaine. Postoperative nausea also was treated preemptively in the outpatient group with the addition of dexamethasone (Decadron) and ondansetron (Zofran), whereas the control patients were treated as needed. Patient charts were reviewed for demographic information, technical aspects, length of donor-site incision, bone graft volume, and time of operation. A Fisher's exact test was used for statistical analysis. Complications including morbidity, readmission, and reoperations were recorded.
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No significant difference was found between the groups regarding early postoperative nausea or vomiting (p > 0.05). However, a significant difference (p < 0.05) was noted in both late postoperative nausea (control: 30% vs. study group: 20%) and late postoperative vomiting (control: 17% vs. study group: 8%).
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We analyzed 68 responses, distributed as follows: Belgium N = 10, France N = 37, The Netherlands N = 7, and Switzerland N = 14. Oral rehydration with ORS was the first line of treatment for 90% of the respondents. In case of first line treatment failure, intravenous rehydration was preferred by 95% of respondents from France, whereas nasogastric route was more likely to be used by those from Belgium (80%), The Netherlands (100%) and Switzerland (86%). Serum electrolyte measurements were more frequently prescribed in France (92%) and Belgium (80%) than in The Netherlands (43%) and Switzerland (29%). Racecadotril was more frequently used in France, and ondansetron was more frequently used in Switzerland. No respondent suggested routine use of antibiotics.
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After one lead-in week of single-blind placebo administration, subjects underwent 11 weeks of double-blind outpatient treatment using a 2 x 4 factorial design that examined age of onset (EOA versus LOA) and medication dose (placebo, or ondansetron 1, 4, or 16 microg/kg twice daily) combined with weekly standardized group cognitive-behavioral therapy. The placebo lead-in week was used to adjust for study entrance effects but not for excluding subjects. Assessments of mood were performed by using the overall score and subscales of the Profile of Mood States both at screening and at weekly intervals during the study.
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Ondansetron (GR 38032) has potent and highly selective antagonist properties at the 5-hydroxytryptamine (5-HT, serotonin) 5-HT3 receptor. The selectivity ratio for ondansetron on 5-HT3 receptors compared with actions on other neurotransmitter receptor types is greater than 1,000. The antiemetic properties of ondansetron have been determined in ferrets against the nausea and vomiting induced by cisplatin, cyclophosphamide, and whole-body radiation. Ondansetron (intravenous 0.01 to 0.1 mg/kg or subcutaneous 0.1 to 0.5 mg/kg) or metoclopramide (1.0 to 4.0 mg/kg) cause dose-dependent inhibitions of the vomiting induced by each of these procedures. Unlike ondansetron, the effects of metoclopramide are accompanied by moderate to marked behavioral depression. Since metoclopramide is 50 times more potent on dopamine D2 receptors than on 5-HT3 receptors, the behavioral depression is likely due to profound blockade of dopamine receptors. The 5-HT3 receptors have been shown to be present peripherally on vagal afferent fibers and are densely located in the vomiting center of the hindbrain. The current hypothesis is that there may be both a peripheral and a central site of action for ondansetron and other 5-HT3 antagonists. The lack of antagonist activity on dopamine and other non-5-HT3 receptors indicates that, unlike metoclopramide, ondansetron will not cause extrapyramidal or other dose-limiting side effects.
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Patients assigned to receive droperidol [Proportional odds ratio: 0.45 (95% confidence interval 0.23-0.88)] reported less pruritus than those who received metoclopramide. Ondansetron effect was similar to metoclopramide [Proportional odds ratio: 0.95 (95% confidence interval 0.49-1.83)]. The NNT for droperidol and ondansetron was 4.0 and 14.7, respectively.
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The American College of Obstetricians and Gynecologists recommends early treatment of nausea and vomiting of pregnancy to stop progression to hyperemesis gravidarum. Nausea and vomiting and hyperemesis gravidarum typically occur during the first trimester, the sensitive time for exposure to teratogens because organogenesis is occurring in the embryo. An efficacious treatment used widely across the United States for both nausea and vomiting of pregnancy and hyperemesis gravidarum is ondansetron. Recent studies have provided conflicting findings on the safety of ondansetron during pregnancy. There are numerous limitations in the current literature on ondansetron safety including exposure to the medication is not limited to sensitive windows of organogenesis, there is a lack of information on dosing and compliance, self-reports of exposure are commonly used, an inadequate accounting exists for other factors that may explain the relationship between ondansetron exposure and the adverse outcome, and there exists a lack of biologic plausibility by which ondansetron might cause harm. It is the authors' opinion that current data do not support a reluctance to treat women with ondansetron in clinical practice.
Ondansetron with dexamethasone group was more effective in controlling PONV after thyroidectomy compared to clonidine with dexamethasone group. However, ramsay sedation scores and total time of analgesia were higher with clonidine than ondansetron.
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In a prospective randomized double-blind study, we compared the effectiveness of dexamethasone 8 mg with either granisetron 1 mg or ondansetron 4 mg in the prevention of postoperative nausea and vomiting in patients undergoing laparoscopic surgery. Hundred ASA I and II patients scheduled for laparoscopic surgery were enrolled in the study and 84 patients completed it. Following induction of anesthesia, group I (n=42) received granisetron 1 mg and dexamethasone 8 mg, group II (n=42) received ondansetron 4 mg and dexamethasone 8 mg. Nausea and vomiting episodes, pain scores as well as side effects were recorded during the first hour and subsequently during the first 6 and 24 hours postoperatively. Satisfaction scores were obtained at discharge. There was no statistically significant difference between the 2 groups during the 1st 24 hours following surgery in regards to pain scores, satisfaction and side effects manifestations. At 0-1 hour interval, 100% of patients in group I and 97.6% in group II had no vomiting. Total response (no moderate or severe nausea and no rescue antiemetics) was 83.3% in group I and 80.95% in group II, and metoclopramide was used in 7.1% of patients in both groups. At 1-6 hours interval, 97.6% of patients in group I and 100% in group II had no vomiting. Total response was 92.8% in group I and 90.9% in group II, and metoclopramide was used in 4.76% of patients in group I and 2.38% in group II. At 6-24 hours no vomiting occurred in 97.6% of patients in group I and 100% in group II. Total response was 95.2% in both groups, and metoclopramide was used in 2.38% of patients in both groups. In conclusion, the combination of dexamethasone 8 mg with either granisetron 1 mg or ondansetron 4 mg following induction of anesthesia in patients undergoing laparoscopic surgery showed no statistically significant difference in antiemetic efficacy with minimal side effects and excellent patient satisfaction.
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GR38032F is a highly selective 5HT3-receptor antagonist which inhibits vomiting induced by cisplatin, cyclophosphamide or X-radiation in the ferret. Since cisplatin selectively increased the levels of 5HT and 5HIAA in the intestinal mucosa, a possible site of the antiemetic action of GR38032F may be on 5HT3-receptors on vagal afferents in the small intestine. The potent antiemetic action of GR38032F should be of clinical value in reducing the nausea and vomiting associated with radiotherapy or chemotherapy of cancer.
Morphine consumption was not significantly different between groups (P=0.085). Overall pain scores were improved in the combination group as compared with the control group both at rest (P=0.042) and during mobilization (P=0.027). In the combination group, individual pain score above 30 mm on a 100 mm visual analogue scale was almost eliminated. The incidence of side effects did not differ between the groups.
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The aim of this analysis was to assess the potential risk for selected cardiac adverse events associated with dolasetron, ondansetron, and granisetron use.
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Nociception was assessed by the radiant heat tail-flick and plantar incision test in male Balb-C mice (25-30 g). The serotonergic pathways were lesioned with an intrathecal injection of 5,7-dihydroxytryptamine. The selective 5-HT7, 5-HT2, and 5-HT3 antagonists; SB-269970 and SB-258719; ketanserin and ondansetron were given intrathecally.
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In humans, the head-up tilted position results in central hypovolaemia which mimicks haemorrhage and is associated with cardiovascular changes that can be divided into two stages. 1) One stage with increase in HR and vascular resistance and a slight increase in MAP. 2) Another stage with decrease in HR, vascular resistance and MAP and appearance of presyncopal symptoms (hypovolaemic shock). The first stage is "sympathoexcitatory" as plasma NA originating from postganglionic vasoconstrictory sympathetic neurons increase. Limb vascular resistance contributes to the increase in TPR at this time. The second stage is "sympathoinhibitory" in nature as plasma NA slightly decreases, or remains unchanged, while plasma A, originating from the adrenal medulla, raises. This pattern is a reflection of a differentiated sympathetic response as an increase in the activity of the nerves innervating the adrenals and decrease in renal sympathetic nerves has been reported by others. There is a decrease in limb as well as total vascular resistance. The secretion of potent vasoactive peptides may contribute to the circulatory changes taken place during head-up tilt. The head-up tilted position is associated with central hypovolaemia which is reliably monitored by electrical impedance. There is a close relation between the increase in thoracic electrical impedance and the decrease in plasma ANP which is regulated by atrial stretch. Also, from recording of technetium labeled red blood cells and measurements of haematocrite the decrease in CBV is reflected by thoracic electrical impedance. In contrast, CVP reflects changes in CBV during the initial head-up tilt only, whereafter CVP usually is unchanged or may even increase. After the initial head-up tilt the decrease in the CBV is caused by further reduction in plasma volume as shown by increase in haematocrite and unchanged distribution of labeled red blood cells. This mechanism is reflected by application of regional electrical impedance measurements at a low and high frequency current. The low frequency current, passing extracellular fluid only, changing more than the high frequency current that passes extra as well as intracellular fluid. Central hypovolaemia was found to stimulate the pituitary-adrenal axis, and the development of hypotension strongly increases plasma ACTH, beta-END, cortisol and PRL. Blocking histaminergic receptors did not change the pituitary-adrenal response to central hypovolaemia, while the sympathoadrenal response was affected by histaminergic receptor blockade. The H2-receptor antagonist cimetidine inhibited plasma A, while the H1-receptor antagonist mepyramine attenuated plasma NA and reduced cardiovascular tolerance, and also induced some sedation. A possible effect of sedation and anxiolysis was investigated by administration of the GABAergic drug diazepam. This drug did not change the cardiovascular response to head-up tilt, but reduced the increase in plasma cortisol. This indicates that the appearance of presyncopal symptoms is not related to "stress" but associated with the cardiovascular effects of central hypovolaemia. Another endogenous substance, serotonin (5-HT), may be also involved in cardiovascular as well as endocrine regulation. We investigated the effect of blocking three main receptors on the development and effects of hypovolaemic shock. Methysergide (5-Ht1+2-receptor antagonist) attenuated plasma NA, beta-END, PRL and PRA during tilt with a slight reduction of cardiovascular tolerance. The 5-HT2-receptor antagonist ketanserin reduced cardiovascular tolerance without significant effects on the hormonal responses. The 5-HT3-receptor antagonist ondansetron inhibited the plasma CGRP and adrenalin response to central hypovolaemia without influencing cardiovascular tolerance. It is concluded that the head-up tilted model in humans can be applied to study cardiovascular and endocrine mechanisms until the development of hypovolaemic shock.(ABSTRACT TRUNCATED)
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The effect of 5-HT receptor agonists and antagonists to inhibit [3H]5-HT uptake was investigated in rat cortical synaptosomes. The 5-HT (5-hydroxytryptamine) uptake inhibitors paroxetine and fluoxetine yielded pKi values of 8.41 +/- 0.12 and 7.43 +/- 0.06 respectively. The 5-HT3/5-HT4 receptor antagonist tropisetron and the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) had similar inhibitory potencies to cocaine (pKi values of 6.58 +/- 0.04, 6.47 +/- 0.14 and 6.45 +/- 0.12 respectively). The dopamine and noradrenaline uptake inhibitors GBR12909 and desipramine had comparable values of 6.5 +/- 0.05 and 6.13 +/- 0.07. Other 5-HT receptor ligands had pKi values less than 6.0 (R(+)-zacopride, MDL72222, R(+)/S(-)-zacopride) or 5.0 (5-methoxytryptamine, m-chlorophenylbiguanide, S(-)-zacopride, SDZ205-557, ondansetron and renzapride). It is concluded, with the possible exception of tropisetron and 8-OH-DPAT, that it is unlikely that the effects of the 5-HT receptor ligands to inhibit 5-HT uptake contribute to their effects in vivo.
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