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:
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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The Authors present their experience in the use of ondansetron in 47 patients receiving 186 cycles of chemotherapy for breast or genital neoplasms.
Nine hundred and twenty-two patients receiving general anaesthesia for major abdominal surgery were assigned to receive a single preoperative dose of oral aprepitant 40 mg, oral aprepitant 125 mg, or i.v. ondansetron 4 mg in a randomized, double-blind trial. Vomiting episodes, use of rescue therapy, and nausea severity (verbal rating scale) were documented for 48 h after surgery. Primary efficacy endpoints were complete response (no vomiting and no use of rescue therapy) 0-24 h after surgery and no vomiting 0-24 h after surgery. The secondary endpoint was no vomiting 0-48 h after surgery.
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Chemotherapy-induced nausea and vomiting is problematic in paediatric brain tumour treatment protocols which often discourage the use of corticosteroids as anti-emetics. The dopamine receptor antagonist, metopimazine, is an effective anti-emetic in combination with ondansetron in adults. The present study was designed to assess its efficacy in children with cancer, a group in which it has not been studied previously.
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Compared with placebo, ondansetron (4 microg/kg b.i.d.) was associated with significant reductions in overall craving in EOA but not LOA, presumably by ameliorating serotonergic abnormality.
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To evaluate the efficacy of antiemetic prophylaxis with ondansetron administered before major ambulatory surgery.
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Analgesic effects of serotonin (5-hydroxytryptamine [5-HT]) type 3 (5-HT3) receptors may involve the release of gamma-aminobutyric acid (GABA) in the spinal dorsal horn. However, the precise synaptic mechanisms for 5-HT3 receptor-mediated spinal analgesia are not clear. In this study, we investigated whether GABAergic neurons in the superficial dorsal horn (SDH) express functional 5-HT3 receptors and how these 5-HT3 receptors affect GABAergic inhibitory synaptic transmission in the SDH, by using slice preparations from adult glutamate decarboxylase 67-green fluorescent protein (GAD67-GFP) knock-in mice. Tight-seal whole cell recordings from GFP-positive and -negative neurons showed that 5-HT3 receptor-specific agonist 2-methyl-serotonin (2-Me-5-HT) induced inward currents in a substantial population of both GFP-positive and -negative neurons. Additionally, we confirmed expression of 5-HT3 receptors in both types of neurons by single-cell reverse transcription-polymerase chain reaction (RT-PCR) analysis. Further, GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs)-both those evoked by electrical stimulation and those occurring spontaneously in tetrodotoxin (i.e., miniature IPSCs [mIPSCs])-were recorded from GFP-negative neurons. 2-Me-5-HT increased the amplitude of the evoked IPSCs and the frequency of mIPSCs. The amplitude of mIPSCs was not affected by 2-Me-5-HT, suggesting that 5-HT augments GABAergic synaptic transmission via presynaptic mechanisms. The present observations indicate that 5-HT3 receptors are expressed on both somadendritic regions and presynaptic terminals of GABAergic neurons and regulate GABAA receptor-mediated inhibitory synaptic transmission in the SDH. Taken together, these results provide clues for the underlying mechanisms of the antinociceptive actions of 5-HT3 receptors in the spinal dorsal horn.
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Lycorine is the main alkaloid of many Amaryllidaceae and known to cause poisoning with still unknown mechanisms. Longer lasting toxicological core symptoms of nausea and emesis may become a burden for human and animal patients and may result in substantial loss of water and electrolytes. To optimise the only empirical symptomatic antiemetic drug treatment at present, it is important to elucidate the causative involved targets of lycorine-induced emesis. Therefore, in the current study, we have tested the actions of a various antiemetic drugs with selective receptor affinities on lycorine-induced nausea and emesis in vivo in dogs. Beagle dogs were pre-treated in a saline vehicle-controlled crossover and random design with diphenhydramine, maropitant, metoclopramide, ondansetron or scopolamine prior lycorine administration (2 mg/kg subcutaneously). In vivo effects were assessed by a scoring system for nausea and emesis as well as by the number and lag time of emetic events for at least 3 h. Moreover, plasma pharmacokinetic analysis was carried out for ondansetron before and after lycorine injection. The data show that histaminergic (H₁), muscarinic and dopaminergic (D₂) receptors are presumably not involved in lycorine-induced emetic effects. While ondansetron significantly reduced the number of emetic events, lycorine-induced emesis was completely blocked by maropitant. Only ondansetron also significantly decreased the level of nausea and was able to prolong the lag time until onset of emesis suggesting a preferential participation of 5-HT₃ receptors in lycorine-induced nausea. Thus, it is the first in vivo report evidencing that predominantly neurokinin-1 (NK₁) and to a lesser extent 5-hydroxytryptamine 3 (5-HT₃) receptors are involved in lycorine-induced emesis facilitating a target-oriented therapy.
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The present study, using the in vivo intracerebral microdialysis method, investigated the role of different serotonin receptor subtypes in the control of dopamine (DA) release exerted by serotonin (5-HT) in the striatum of halothane-anesthetized rats. Striatal dialysate DA content was reduced following the blockade of voltage-dependent Na+ channels by tetrodotoxin or by the removal of Ca2+ from the perfusion medium, and increased following depolarization with K+ ions. These findings demonstrate that under our experimental conditions, DA content reflects the neuronal origin of the neurotransmitter release. Drugs were locally applied by means of the microdialysis probe. One, 2.5 and 5 microM 5-HT significantly enhanced DA release in a concentration-dependent manner up to 157, 253 and 446% of basal values respectively. The effect induced by 1 microM 5-HT was not blocked by 10 microM (-)pindolol, a 5-HT1 receptor antagonist, 1 microM ketanserin or 10 microM cinanserin, both 5-HT2A antagonists. One or 10 microM ondansetron (GR 38032F), a selective 5-HT3 antagonist, were also ineffective. In contrast, 10 or 100 microM DAU 6285, a 5-HT3/4 antagonist, significantly reduced the effect of 5-HT on DA release (-20% and -60% respectively). Moreover, 100 microM BIMU 8, a selective 5-HT4 agonist, enhanced DA release (+85%) and this effect was reduced by 100 microM DAU 6285 (-40%). These results demonstrate that in vivo 5-HT exerts a facilitatory influence on striatal DA release and that the 5-HT4, but not the 5-HT1, 5-HT2 or 5-HT3, receptor subtype is implicated, at least partially, in this effect.
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Since its introduction in 1991, ondansetron has become a commonly used antiemetic in US academic medical centers. Although ondansetron is safe and effective in improving patients' tolerance of emetogenic therapies, including cancer chemotherapy, its high cost has added a significant burden to the pharmaceutical budgets of many institutions. The study data suggest that compliance with ondansetron prescribing guidelines, with elimination of indiscriminant use, could result in significant cost savings.
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We analyzed data from a prospective clinical trial performed between January 2004 and April 2005. Data were collected on 105 children with dehydration due to gastroenteritis who received an ondansetron oral disintegrating formulation. The following outcomes of efficacy were analyzed: number of vomiting episodes, volume of oral rehydration fluids consumed, percent weight gain, and the proportions of children who had ongoing vomiting, received intravenous rehydration, and were hospitalized. In addition, the number of episodes of diarrhea was evaluated to measure whether there were dose-dependent side effects.
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24-72 h after cisplatin administration, in the middle dose Armillariella tabescens group, the high dose Armillariella tabescens group and the ondansetron group, the kaolin intake was significantly lower than that in the model group, respectively (P<0.05). The most significant difference was between the high dose Armillariella tabescens group [(0.58 +/- 0.23) g/24 h] and the control group [(2.16 +/- 0.98) g/24 h] at 24 h after cisplatin administration. The variables, such as consumption of food during 48-72 h (P<0.05), water during 48-72 h (P<0.05), and body weight at 72 h (P<0.05) in the middle dose Armillariella tabescens group were significantly higher than those in the model group, but no statistically significant difference between the ondansetron group and the model group (P>0.05).
Combinations of dopamine antagonists or high-dose metoclopramide with steroids can provide complete control of chemotherapy-related nausea and vomiting in up to 60-70% of patients undergoing high-dose cisplatin-based chemotherapy. High-dose metoclopramide probably acts as a 5-HT3 receptor antagonist, but because of its dopamine-receptor antagonism it is the cause of extrapyramidal side-effects. These compounds, and the agents used in combination with them, tend to cause sedation, an undesirable effect in the outpatient setting. Specific 5-HT3 receptor antagonists (ondansetron, granisetron, tropisetron) give a similar control of chemotherapy related nausea and vomiting, with minimum side-effects. These drugs can cause headaches and constipation and some have been related to transient liver enzyme abnormalities in cancer patients; however, disease and chemotherapy might also be the cause of the enzyme anomalies. Combinations of 5-HT3 receptor antagonists with steroids may provide a very high degree of protection.
A randomized, double-blind, placebo-controlled study was designed to compare the relative efficacy of prophylactic ondansetron, 4 mg intravenously (IV), when administered before induction of anesthesia or at the end of surgery to an outpatient population at high risk of developing postoperative nausea and vomiting (PONV). Patients undergoing otolaryngologic surgery were randomly assigned to one of three different treatment groups: Group 1 (placebo) received saline 5 mL prior to induction of anesthesia and again at the end of surgery; Group II received ondansetron 4 mg in 5 mL prior to induction of anesthesia and saline 5 mL at the end of surgery; and Group III received saline 5 mL prior to induction of anesthesia and ondansetron 4 mg at the end of surgery. All patients received the same general anesthetic technique. A standardized regimen of rescue antiemetics was administered in the recovery room to patients with > or = 2 emetic episodes or at the patients request for persistent nausea. Episodes of nausea and vomiting, as well as the need for rescue antiemetics, were recorded for 24 h after the operation. The incidences of nausea and emesis in the recovery room after prophylactic ondansetron, 4 mg IV, administered either before induction (68% and 20%, respectively) or at the end of surgery (60% and 4%, respectively) were not significantly decreased compared to the placebo control group (80% and 12%, respectively). However, when ondansetron was administered at the end of the operation, it significantly reduced the need for rescue antiemetics in the recovery room (36% vs 64% in the control group). The postanesthesia care unit and hospital discharge times were similar in all three study groups. One patients in Group II and one patient in Group III were hospitalized because of intractable symptoms related to PONV. After discharge from the ambulatory surgery unit, the incidence of nausea, vomiting, and the need for rescue antiemetic drugs were similar in all three treatment groups. In conclusion, ondansetron (4 mg IV) was more effective in reducing the need for rescue antiemetics in the recovery room when administered at the end versus prior to the start of otolaryngologic surgery. Therefore, when ondansetron is used for antiemetic prophylaxis in outpatients undergoing otolaryngologic procedures, it should be administered at the end of the operation rather than prior to induction of anesthesia.
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In this study we tested the hypothesis that tapentadol inhibits GGRP release from the rat brainstem through a mechanism mediated by the inhibition of NA reuptake; as a second alternative hypothesis, we investigated whether tapentadol inhibits GGRP release via the inhibition of 5-HT reuptake.
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The incidences of nausea and vomiting in ondansetron group(33.3% and 26.7%) were significantly lower than those in placebo group(73.3% and 66.7%) (P < 0.05). Administration of ondansetron had no obvious effect on the mean arterial pressure, SpO2, and respiratory frequency.
In the murine colon, local RAS may play a significant role in the control of contractile activity. Ang II positively modulates the spontaneous contractile activity via activation of post-junctional and pre-junctional AT(1A) receptors, the latter located on the enteric neurones, modulating the release of tachykinins and acetylcholine.
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The 5-HT3 receptor antagonist tropisetron (ICS 205-930) was found to be a potent and selective partial agonist at alpha7 nicotinic receptors. Two other 5-HT3 receptor antagonists, ondansetron and LY-278,584, were found to lack high affinity at the alpha7 nicotinic receptor. Quinuclidine analogues (1 and 2) of tropisetron were also found to be potent and selective partial agonists at alpha7 nicotinic receptors.
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For effective postoperative antiemetic management in pediatric moyamoya disease patients receiving fentanyl based postoperative analgesia, a multimodal approach has been recommended. The uncertain efficacy of ondansetron for pediatric neurosurgical patients or the possible antiemetic effect of small dose of propofol motivated us to evaluate the preventive effect of a subhypnotic dose of propofol combined with dexamethasone on postoperative vomiting (POV), especially during immediate postoperative periods.
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A total of 75 anesthesiologist status I/II patients undergoing elective craniotomy for brain tumors were randomized into three groups, G, O and D, to receive single doses of dexamethasone 8 mg at induction with either granisetron 1 mg, ondansetron 4 mg or normal saline 2 ml at the time of dural closure respectively. Episodes of nausea, retching, vomiting and number of rescue antiemetic (RAE) were noted for 48 h post-operatively.
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Although we acknowledge that subset numbers in this post hoc analysis may be too small to allow definitive conclusions, the data suggest that aprepitant triple therapy provides a benefit over control therapy for the prevention of CINV in patients receiving anthracycline and cyclophosphamide (AC)- or non-AC-based moderately emetogenic chemotherapy across age, gender, and region. (Original trial results available at ClinicalTrials.gov: NCT00337727.).
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Thrombocytopenia was excessive in early cohorts with a carboplatin dose of 400 mg/m2, but was minimal at lower doses. Other toxicity was generally tolerable and reversible, particularly at carboplatin doses < or = 300 mg/m2, although gastrointestinal and neurological toxicity tended to worsen as additional modulators were added. No major responses (but 4 minor responses) were seen in this patient population with heavily pretreated or primarily resistant cancers.
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Vortioxetine increased wakefulness and increased frontal cortical activity, most likely because of its 5-HT7 and 5-HT3 antagonism and 5-HT1A agonism. Vortioxetine differs from escitalopram and duloxetine by increasing cortical θ, α and γ oscillations. These preclinical findings suggest a role of vortioxetine in modulating cortical circuits known to be recruited during cognitive behaviours and warrant further investigation as to their clinical impact.
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