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Zofran (Ondansetron)
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Zofran

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:

Similar Products:
Dexamethasone, Scopolamine, Anzemet

 

Also known as:  Ondansetron.

Description

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.

Dosage

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.

Overdose

If you overdose Generic Zofran and you don't feel good you should visit your doctor or health care provider immediately.

Storage

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.

Side effects

The most common side effects associated with Zofran are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

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.

Avoid alcohol.

Do not stop taking Generic Zofran suddenly.

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Of 703 patients enrolled, 696 were eligible. There were 343 dolasetron- and 353 ondansetron-treated patients; 57% of dolasetron-treated patients had complete protection in the first 24 hours versus 67% of patients who received ondansetron (P = .013). MNS was also more pronounced on the dolasetron arm (P = .051). Sixty-seven percent of patients who received added dexamethasone in the first 24 hours had complete protection, compared with 55% without dexamethasone (P < .001). MNS was significantly reduced with the addition of dexamethasone (P < .001). At 7 days, dolasetron and ondansetron had equivalent complete protection rates (36% and 39%, respectively). With the addition of dexamethasone, 48% of patients compared with 28% had complete protection (P < .001). MNS was significantly improved with added dexamethasone (P < .001).

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This retrospective evaluation included patients who were admitted to the cardiac ICUs between January 2009 and July 2009 aged ≥ 18 years with electrocardiographic evidence of a QTc ≥ 500 ms. Patients receiving at least two concomitant drugs known to prolong the QT interval were considered to experience a pharmacodynamic DDI. Drugs causing CYP450 inhibition of the metabolism of QT prolonging medications were considered to cause pharmacokinetic DDIs. The causality between drug and QTc prolongation was evaluated with an objective scale.

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Participated in these study 100 patients scheduled for non-obstetric procedures, who were randomly distributed in five groups: control (no treatment - C); 2.5 mg droperidol (D); 10 mg nalbuphine (N); association of previous drugs (DN); and 8 mg ondansetron (O). Pruritus was quantitatively evaluated at 30 minutes, 1, 2 and 3 hours after spinal sufentanil.

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We studied 484 women at high risk for developing PONV scheduled to undergo operations associated with high emetogenic risk.

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Patients received either dexmedetomidine 0.5 μg kg⁻¹ i.v. (dexmedetomidine group) or 0.9% normal saline (control group) 30 min before the completion of surgery followed by fentanyl 0.5 μg kg⁻¹ and 4 mg ondansetron. Postoperatively, the PCA (fentanyl 10 μg kg⁻¹ with 120 mg ketorolac, with or without dexmedetomidine 10 μg kg⁻¹ made up to a total volume of 100 ml) was programmed to deliver 1 ml bolus (lockout 15 min) with a continuous background infusion of 2 ml h⁻¹. The PCA was used for the first 48 h postoperatively.

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The patients were due for laparoscopic Roux-en-Y gastric bypass and enteral bypass. Sleep was induced after pre-oxygenation with target control infusions (TCI) of remifentanil and propofol; vecuronium was supplied for facilitating endotracheal intubation. The propofol infusion was stopped and desflurane 3-6% was given for BIS-titrated anaesthetic maintenance together with remifentanil TCI. Antiemetic prophylaxis was supplied with intravenous (IV) droperidol, ondansetron and dexamethasone; post-operative pain prophylaxis was IV paracetamol, parecoxib and bupivacaine infiltration. The patients were extubated in the operating room and kept in the post-operative care unit for 3-4 h, being tested for a 20 m walk before discharge to the ward.

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Patients undergoing general anesthesia for laparoscopic cholecystectomy are at high risk for postoperative nausea and vomiting (PONV). This study compared ramosetron and ondansetron in terms of efficacy for PONV prevention after laparoscopic cholecystectomy.

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Several medication strategies can be considered as promising alternatives or augmenting to antidepressant or benzodiazepine therapy in GAD.

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The two schedules of ondansetron used in the first 24 hours were no different in their antiemetic efficacy, with similar rates for complete responses (76.7% v 72.0%, P = .472), complete plus major responses (90.2% v 82.0%, P = .135), and severity of nausea (P = .348). Oral ondansetron after 24 hours was more effective than placebo in preventing delayed nausea and emesis, with superior rates of complete responses (59.6% v 42.1%, P = .012 by one-sided test), complete plus major responses (80.9% v 66.3%, P = .018 by one-sided test), and less severe nausea (9.2 mm v 18.6 mm on a 100-mm VAS, P = .002). The efficacy of ondansetron was maintained over subsequent courses of chemotherapy.

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Serotonin and 5-HT3 receptors may be involved in the activation of nociceptive afferent pathways by rectal distension. In rats, intracolonic infusion of glycerol is able to trigger nociceptive inputs as evidenced by the occurrence of abdominal constrictions. This work was designed to evaluate the influence of 5-HT3 receptor antagonists on this reflex and to approach the site of action by comparing their relative efficacies according to the route of administration. Male Wistar rats (250-350 g) were surgically prepared for abdominal electromyography and a catheter was placed in the colonic lumen. Five days after surgery, electrical activity of abdominal muscles was recorded before and during (20 min) intracolonic infusion of glycerol (60% glycerol + 40% saline, rate 0.75 mL/h). Cilansetron was administered intraperitoneally, 15 min before glycerol infusion, at doses of 5 to 500 micrograms/kg. Granisetron, ondansetron and cilansetron were administered at the dose of 20 micrograms/kg by intraperitoneal (i.p.), intravenous (i.v.) or intracolonic (i.c.) routes. The number of abdominal spike bursts was used as an index of visceral nociception. Intracolonic infusion of glycerol increased significantly (P < 0.05) the number of abdominal spike bursts during the time of infusion compared with saline (30.6 +/- 6.6 vs 4.5 +/- 3.4 bursts). When administered i.p., cilansetron dose-dependently reduced the frequency of abdominal spike bursts from the dose of 20 micrograms/kg i.p. Administration i.p. of granisetron and ondansetron at this dose also significantly reduced the number of abdominal spikes (19.0 +/- 6.0 and 18.3 +/- 6.9 respectively). Cilansetron, ondansetron and granisetron were also effective by i.v. and i.c. routes, cilansetron was more active by the i.c. route. Serotonin, via 5-HT3 receptors, is involved in the mediation of abdominal contractions induced by intracolonic infusion of glycerol. 5-HT3 receptor antagonists are also active by i.c. route suggesting a local site of action.

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The involvement of opioid receptor activation in the antinociceptive effect of either fluvoxamine, a selective serotonin reuptake inhibitor, or serotonin (5-HT) on thermal hyperalgesia and mechanical allodynia in a model of neuropathic pain in mice induced by sciatic nerve ligation was examined. The experiments were conducted 2 or 6 weeks after unilateral sciatic nerve ligation. Ipsilateral thermal hyperalgesia and mechanical allodynia were observed both 2 and 6 weeks after sciatic nerve ligation. Neither s.c. fluvoxamine nor i.t. 5-HT affected sciatic nerve ligation-induced thermal hyperalgesia or mechanical allodynia in mice 2 weeks after sciatic nerve ligation. However, the same dose of either fluvoxamine or 5-HT significantly reduced mechanical allodynia but not thermal hyperalgesia in sciatic nerve ligated mice 6 weeks after surgery. The antinociceptive effect of fluvoxamine on sciatic nerve ligation-induced mechanical allodynia in mice 6 weeks after surgery was completely abolished by pretreatment with either naloxone, a nonselective opioid receptor antagonist, or beta-funaltrexamine, a selective mu-opioid receptor antagonist. Furthermore, pretreatment with naltrindole, a selective delta-opioid receptor antagonist, partially but significantly inhibited the antinociceptive effect of fluvoxamine in sciatic nerve ligated mice at the 6th postoperative week. The antinociceptive effect induced by i.t. 5-HT was also completely antagonized by either naloxone or beta-funaltrexamine, and partially inhibited by naltrindole. However, pretreatment with nor-binaltorphimine, a selective kappa-opioid receptor antagonist, had no effect against either s.c. fluvoxamine- or i.t. 5-HT-induced antinociception. These results suggest that the antinociceptive effect of s.c. fluvoxamine or i.t. 5-HT in the chronic state of sciatic nerve ligation-induced neuropathic pain may be related to opioidergic activity, mainly through the activation of spinal mu- and delta-opioid receptors.

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Although restraint stress accelerates colonic transit via a central corticotropin-releasing factor (CRF), the precise mechanism still remains unclear. We tested the hypothesis that restraint stress and central CRF stimulate colonic motility and transit via a vagal pathway and 5-HT(3) receptors of the proximal colon in rats. (51)Cr was injected via the catheter positioned in the proximal colon to measure colonic transit. The rats were subjected to a restraint stress for 90 min or received intracisternal injection of CRF. Ninety minutes after the administration of (51)Cr, the entire colon was removed, and the geometric center (GC) was calculated. Four force transducers were sutured on the proximal, mid, and distal colon to record colonic motility. Restraint stress accelerated colonic transit (GC of 6.7 +/- 0.4, n=6) compared with nonrestraint controls (GC of 5.1 +/- 0.2, n=6). Intracisternal injection of CRF (1.0 microg) also accelerated colonic transit (GC of 7.0 +/- 0.2, n=6) compared with saline-injected group (GC of 4.6 +/- 0.5, n=6). Restraint stress-induced acceleration of colonic transit was reduced by perivagal capsaicin treatment. Intracisternal injection of CRF antagonists (10 microg astressin) abolished restraint stress-induced acceleration of colonic transit. Stimulated colonic transit and motility induced by restraint stress and CRF were significantly reduced by the intraluminal administration of 5-HT(3) antagonist ondansetron (5 x 10(-6) M; 1 ml) into the proximal colon. Restraint stress and intracisternal injection of CRF significantly increased the luminal content of 5-HT of the proximal colon. It is suggested that restraint stress stimulates colonic motility via central CRF and peripheral 5-HT(3) receptors in conscious rats.

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A total of 82 patients were enrolled, 39 received ropivacaine, and 43 received placebo. There was no statistically significant difference in narcotic usage between the ropivacaine group and placebo group, 51.9 mg versus 55.2 mg, respectively (P = .63). Ondansetron usage was 10.7 mg and 10.6 mg for ropivacaine and placebo groups. (P = .98). Average pain score was 3.0 for each group (P = .632). Total hospital length of stay was 37.5 hours for ropivacaine group and 38.1 hours for placebo group (P = .768).

zofran dose pediatrics

Sixty-four patients completed the study (n = 28 in the control group, n = 36 in the intervention group). In the control group, 36% of the patients reached their preoperative activity level after 1 week, as compared to 50% in the intervention group (p = 0.19). Resumption of daily physical activity during the first postoperative week in the intervention group was not significantly different from the control group [repeated measures analysis of variance (MANOVA), p = 0.05]. However, in contrast with men, women in the intervention group did show a faster recovery of daily physical activity as compared to the control group (MANOVA, p = 0.02). Although there was no significant difference in postoperative VAS scores for pain and nausea between both groups, patients in the intervention group experienced pain less often as a limiting factor (p = 0.006).

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The incidence of PONV and use of rescue antiemetics was significantly greater in the ondansetron group compared with the prochlorperazine group. The mean total costs of PONV management per patient in the prochlorperazine and ondansetron groups were dollar 13.99 and dollar 51.98, respectively (based on 2004 average wholesale prices [AWP]). The cost of successfully treating one patient with prochlorperazine and ondansetron was dollar 31.87 and dollar 275.01, respectively. One-way sensitivity analysis was performed adjusting the percent efficacy rate of each antiemetic and the drug cost of ondansetron (up to a 50% reduction in AWP). Prochlorperazine remained the dominant strategy across each scenario.

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Of 100 patients treated with droperidol added in a patient-controlled analgesia pump with morphine, 30 who would have vomited or been nauseated had they not received droperidol will not suffer these effects. There is no evidence of dose-responsiveness for efficacy with droperidol, but the risk of adverse effects is dose-dependent. There is a lack of evidence for other antiemetics.

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1. The anti-emetic effects of the NK1 tachykinin receptor antagonist, CP 99,994 (10 mg kg-1) were investigated in the ferret using a cisplatin-induced acute (day 1) and delayed (day 2 and 3) retching and vomiting model. 2. With a single cisplatin (10 mg kg-1) emetogenic challenge, the i.p. administration of CP 99,994 given as a single injection immediately following the first emetic episode, promptly abolished the retching and vomiting for a 4 h period. CP 99,994 was as efficacious as ondansetron (1.0 mg kg-1). The general toxicity of cisplatin 10 mg kg-1 precluded its use in studies of delayed emesis. 3. With a single cisplatin (5 mg kg-1) emetogenic challenge, the single administration of either CP 99,994 (10 mg kg-1) or ondansetron (1.0 mg kg-1) immediately following the first emetic episode markedly reduced or abolished the retching and vomiting for 4 h. Such single treatments failed to modify significantly the intensity of delayed emesis appearing on the second and third day. 4. With a cisplatin (5 mg kg-1) emetogenic challenge, administration of CP 99,994 (10 mg kg-1) at 8 hourly intervals, the first injection being administered 30 s post cisplatin, was associated with 4 or more abolitions of emesis during both the acute and delayed phase. A 4 hourly administration of CP 99,994 for 20 h during delayed emesis completely abolished the retching and vomiting. 5. It is concluded that cisplatin 5 mg kg-1 provides an emetogenic challenge causing an acute and delayed phase of retching and vomiting and that CP 99,994 can abolish both phases. The results may be relevant to the understanding and treatment of chemotherapy-induced emesis in man.

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To determine the prevalence of substandard antiemetic therapy among recently published trials conducted in patients with cancer who received emetogenic chemotherapy.

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An inspired oxygen fraction of 0.8 during general anesthesia with sevoflurane does not decrease PONV in patients undergoing strabismus repair. Ondansetron also did not significantly decrease PONV in our study setting.

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Palonosetron is comparable to ondansetron for PONV prophylaxis in elective laparoscopic cholecystectomy when administered as single pre-induction dose.

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Promethazine was significantly more effective than ondansetron for treating PONV after failed ondansetron prophylaxis. Promethazine 6.25 mg was as effective as higher doses.

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A statistically significant reduction in postoperative nausea between 8 and 24 hours in patients receiving TDS was noted.

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Nausea and vomiting are well-known gastrointestinal complications in chronic renal failure and are frequent indications for the commencement of dialysis. Although the administration of antiemetic drugs (metoclopramide and, recently, ondansetron) is usually mentioned, there are scanty data on their effects.

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The present study assessed 5-HT3 receptor recognition site levels in homogenates of putamen derived from patients with clinically and neurochemically diagnosed Huntington's disease or Parkinson's disease and those from age-, sex- and post-mortem delay-matched neurologically and psychiatrically normal patients to investigate the cellular location of 5-HT3 receptors in the human putamen. Specific [3H]granisetron (0.91 nM) binding (defined by ondansetron, 10 microM) was significantly reduced in putamen homogenates from eight out of ten patients with Huntington's disease compared to similar homogenates from 'control' patients (72 +/- 6 and 39 +/- 8 fmol/g wet weight, mean +/- S.E.M., n = 10 and 8, tissue from 'control' and Huntington's disease patients, respectively, P = 0.004). In contrast, specific [3H]granisetron (1.04 nM) binding levels were similar in putamen homogenates from patients with Parkinson's disease when compared to homogenates from 'control' patients. The present results indicate that at least a proportion of the 5-HT3 receptor population in the human putamen is located on neurones that have their cell bodies within this brain region and that these receptors are not primarily located on dopamine neurone terminals in the human putamen.

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A prospective, randomized, crossover study was conducted in patients aged 2-18 years. 160 chemotherapy cycles, consisting of chemotherapy drugs with moderate- and high-emetogenic potential, were studied. The study group received a single dose of intravenous (IV) palonosetron 5 mcg/kg, and the standard group received IV ondansetron 5 mg/m2 every 8 hours while receiving chemotherapy. The patients were observed for vomiting, use of rescue antiemetic medications, and nausea from Day 1 0-72 hours after completion of each chemotherapy cycle. All adverse events during the study period were recorded.

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Ondansetron may be the preferred agent for controlling nausea and vomiting in patients with neurosurgical trauma. Controlled clinical trials are needed to evaluate its safety and efficacy in this patient population.

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This study suggests that the use of ondansetron to control CDDP-induced nausea and vomiting does not affect CDDP antitumor efficacy.

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medicine zofran 2016-12-11

The incidence of POV within 24 h postoperative period in each group was P 33%; O 11%, A 9% and C 6%. Outcomes for all intervention groups were significantly better than that for placebo (p<0.01). For the three interventions compared with placebo, the numbers needed to treat (NNTs) were O, NNT=5; A, NNT=5 and C buy zofran , NNT=4. The secondary outcomes also demonstrated greater benefits of the combined regimen, with improvement seen in all the measures.

zofran generic 2016-02-09

Ondansetron attenuates hepatic injury following haemorrhagic shock, which is, buy zofran at least in part, to be due to its anti-inflammatory effect via p38 MAPK signal pathway.

zofran 3 mg 2017-03-06

Total surgical, anesthesia, extubation, and postanesthesia care unit (PACU) occupancy times were recorded along with anesthesia recovery scores. The incidence and severity of nausea, vomiting, and pain along with rescue antiemetic administration, also were recorded. Similar assessments were made over the next 24 hours. Intergroup demographic data were similar except that the male to female ratio was higher in the ondansetron buy zofran group. Stewart scores, reflecting emergence from anesthesia, were higher with ondansetron compared with droperidol. The incidence of nausea was similar between the groups but the severity was less after ondansetron therapy. More patients vomited after placebo than when given either droperidol or ondansetron. No intergroup differences were noted in the use of rescue antiemetics. Twenty-four hours later, more patients who received the placebo drug had nausea or vomited compared with either ondansetron or droperidol.

zofran gel 2015-05-28

Efficacy of 5-HT(3)RAs for preventing CINV following cisplatin- and non-cisplatin-based chemotherapy is comparable, with the exception of granisetron vs tropisetron. Some differences were noted in dosing buy zofran subanalyses.

zofran recommended dosage 2016-07-26

It was a randomized open-label prospective study. Sixty-two patients were randomized to receive either ondansetron 32-mg infusion over 24 h, or olanzapine wafer 10 mg once daily in addition to ondansetron 8 mg IV three times a day or a single dose of palonosetron 0.25 mg IV instead of ondansetron. All groups were allowed rescue antiemetics. The primary endpoint was a composite outcome of no emesis, no use of rescue medication, and nausea score reduction of ≥50 %. The secondary endpoint was nausea score reduction of ≥50 %. Both endpoints buy zofran were measured at 24 and 48 h after initiation of the study treatment. Statistical analysis was conducted using a double-sided Fisher's exact test.

zofran overdose 2015-11-03

Although there is general agreement that mucosal 5-hydroxytryptamine (5-HT) can initiate peristaltic reflexes in the colon, recent studies have differed as to whether or not the role of mucosal 5-HT is critical. We therefore tested the hypothesis that the secretion of 5-HT from mucosal enterochromaffin (EC) cells is essential for the manifestation of murine colonic peristaltic reflexes. To do so, we analysed the mechanisms underlying faecal pellet propulsion in isolated colons of mice lacking tryptophan hydroxylase 1 (Tph1(-/-) mice), which is the rate-limiting enzyme in the biosynthesis of mucosal but not neuronal 5-HT. We used video analysis of faecal pellet propulsion, tension transducers to record colonic migrating motor complexes (CMMCs) and intracellular microelectrodes to record circular muscle activity occurring spontaneously or following intraluminal distension. When compared with control (Tph1(+/+)) mice, Tph1(-/-) animals exhibited: (1) an elongated colon; (2) larger faecal pellets; (3) orthograde propulsion followed by retropulsion (not observed in Tph1(+/+) colon); (4) slower in vitro propulsion of larger faecal pellets (28% of Tph1(+/+)); (5) CMMCs that infrequently propagated in an oral to anal direction because of impaired descending inhibition; (6) reduced CMMCs and inhibitory responses to intraluminal balloon distension; (7) an absence of reflex activity in response to mucosal stimulation. In addition, (8) thin pellets that propagated along the control colon failed to do so in Tph1(-/-) colon; and (9) the 5-HT3 receptor antagonist ondansetron, which reduced CMMCs and blocked their propagation in Tph1(+/+) mice, failed to buy zofran alter CMMCs in Tph1(-/-) animals. Our observations suggest that mucosal 5-HT is essential for reflexes driven by mucosal stimulation and is also important for normal propagation of CMMCs and propulsion of pellets in the isolated colon.

medication zofran 2017-01-21

Selective antagonism of 5-HT3 receptors suppresses the gastric component of phase-3 motor activity and simultaneously suppresses plasma motilin peaks. The results suggest that the buy zofran suppression of gastric activity fronts is achieved via the suppression of plasma motilin peaks because in the presence of ondansetron a motilin agonist like erythromycin restores the gastric phase 3.

zofran nausea medication 2016-08-13

This study was performed in a group of 89 patients treated for breast carcinoma with a FEC regimen (5-fluorouracil, epirubicin, cyclophosphamide). The aim was to evaluate the antiemetic efficacy of one 8 mg tablet ondansetron (OND), and in case of failure, to measure the recovering level by the administration of 8 mg i.v. OND. One tablet of OND was given before the first course. A complete or major control of emetic episodes (EE) (0-2 EE) over the 24 first hours was obtained in 55 patients (62%). A complete or major control of nausea (absent or mild) was obtained in 46 patients (52%). A success, defined as a complete or major control buy zofran for EE and nausea during the first 5 days, was obtained in 36 patients (40%). These 36 patients were treated again with 8 mg oral OND at the second course, with a success level of 61% (22/36). Among the 53 patients unresponsive to the oral OND, 38 were treated by 8 mg i.v. OND at the second course. A complete or major control for EE and for nausea over the first 24 hours was obtained respectively in 11 patients (29%), and 11 patients (29%). No success was obtained. The 15 remaining patients, who had a very bad tolerance at the first course were excluded from the study and treated by OND-methylprednisolon, with only one success obtained. This study shows that the exclusive use of one 8 tablet OND is not sufficient in prevention of emesis induced by a FEC regimen, and that failures are only partially recovered by the i.v. route.

zofran drug interactions 2015-10-25

Ondansetron is a 5-hydroxytryptamine 3-receptor antagonist which has shown activity in the prevention of cytotoxic-induced emesis. Preliminary non-randomized studies also indicated efficacy in preventing sickness following radiotherapy. The present study was therefore undertaken to compare the efficacy and safety of ondansetron (8 mg tds orally) and metoclopramide (10 mg tds orally) in preventing sickness after single-exposure radiotherapy treatments of 8-10 Gy to the upper abdomen. Of 82 evaluable patients 38 received ondansetron and 44 metoclopramide. On the first day after irradiation vomiting or retching was prevented in all but one of the patients on buy zofran ondansetron whereas metoclopramide achieved complete control of these symptoms in only 46% of subjects (P less than 0.001). Similarly nausea was significantly better controlled by ondansetron in the first 24 hours after treatment (P = 0.001). Complete or major control of vomiting or retching was maintained for 92%-100% of patients on ondansetron during the five days of the study period. In the metoclopramide group the proportion of patients with equivalent control improved from 70% on day 1 to 95 on day 5. Both drugs were well-tolerated.

zofran 9 mg 2015-02-11

There are several life threatening deadly diseases in our world but ‘Cancer’ out powers buy zofran them all in recent years. Chemotherapy may be used on its own or an adjunct to other forms of therapy. Despite the advancement in cytotoxic drug therapy and supportive treatment almost 70% of patient suffer from chemotherapy induced nausea and vomiting (CINV). Ondansetron, a 5-HT(3) receptor antagonist has now become a gold standard in the treatment of chemotherapy induced nausea and vomiting. The central actions of ondansetron are well established but its peripheral actions are not well recognized. The aim of our study was to explore the peripheral actions of ondansetron. Experiments were performed in five groups (n=6) and ileal smooth muscles activity was recorded on power lab (USA). The effects of increasing concentrations of acetylcholine, serotonin & ondansetron alone was observed in first three groups. In the next two groups effects of acetylcholine and serotonin pretreated with fixed concentration (1ml) of ondansetron (10¯ϖ M)were studied. The maximum response obtained by acetylcholine served as a control for our study. Maximum response with acetylcholine was taken as 100% and with serotonin was 177 percent of control. Cumulative dose response curve with ondansetron was triphasic. At 10¯ψM it was 28.8%, whereas with 10¯ξM the amplitude decreased to 16.87%, it reached to plateau at 10¯ϖ M. Response of acetylcholine & serotonin was decreased to 57% and 78% respectively in the presence of fixed concentration of ondansetron (10¯ϖ M). Ondansetron reduces the acetylcholine and serotonin induced gastrointestinal motility. Our study has indicated that ondansetron apart from having central action also has marked peripheral actions that play an important role in CINV and may act as a partial agonist.

zofran buy 2015-08-16

A total of 215 patients were entered into the study. Of these, 207 were evaluable (111 previously-untreated and 96 previously-treated patients). In the chemotherapy-naive patients the combination of ondansetron plus dexamethasone was significantly superior to ondansetron plus placebo in protecting the patients completely from emesis (retching and vomiting) (81% versus 64%, p = 0.04). The mean number of vomiting episodes was significantly lower in the ondansetron-plus-dexamethasone-treated patients than in those receiving ondansetron plus placebo (0.8 versus 2.1, p = 0.03). In this group of patients there was significantly superior protection from emesis on the second day (p-value = 0.04), and a trend towards a better protection on the third and fourth days. On each day the active combination offered better protection from nausea with an approximately 20% difference in favor of ondansetron plus dexamethasone. In the group of established vomiters the combination of ondansetron plus dexamethansone was superior to ondansetron plus placebo in protecting the patients from acute emesis, with 70% versus 48% of the patients being completely protected (p = 0.03). The mean number of vomiting episodes was significantly lower in the ondansetron-plus-dexamethasone-treated-patients than in those receiving ondansetron plus placebo (0.9 versus 2.1, p = 0.02). In the ondansetron-plus-dexamethasone arm 55% of the patients had complete protection from nausea, retching and vomiting compared to 35% in the ondansetron-plus-placebo-treated buy zofran group (p = 0.05). Overall 22% of the patients (20% in the ondansetron-plus-placebo and 25% in the ondansetron-plus-dexamethasone arm) experienced at least one, usually mild, adverse event. More patients in the ondansetron-plus-dexamethasone arm complained of epigastric pain or burning (8/101 versus 4/112, p-value = 0.16). The difference in patients reporting constipation (6/101 versus 0/112) was highly significant at a p-value of 0.008.

zofran drug classification 2017-04-18

Postoperative nausea and vomiting (PONV), a common complication after anesthesia and surgery, often results in delayed discharge with the patient's unpleasant symptoms continuing at home. To effectively prevent and treat PONV, it is important to understand the factors implicated in PONV, the mechanisms of PONV, the pharmacology of the antiemetic agents, and the nonpharmacologic measures that have been shown to be effective. The cause of PONV is likely to be multifactorial, with important predictors being female gender, history of PONV, and history of motion sickness. The vomiting center can be triggered by activation of dopamine, serotonin (type 3), histamine (type 1), and muscarinic cholingergic receptors in the chemoreceptor trigger zone and the nucleus tractus solitarus, as well as acetylcholine receptors in the vestibular apparatus, vagal afferents from the periphery, and the endocrine environment. Antiemetic agents such as the serotonin antagonists (eg, ondansetron, dolasetron), droperidol, antihistamines (eg, diphenhydramine, dimenhydrinate), and promethazine can prevent and treat PONV effectively. Transdermal scopolamine and dexamethasone have a role in the prevention of PONV, particularly for certain high-risk patients. Nonpharmacologic measures and alternative treatments such as buy zofran hydration, maintaining blood pressure, acupressure techniques, trancutaneous acupoint stimulation, and isopropyl alcohol must not be overlooked. Finally, an evidence-based algorithm for the prevention and treatment of PONV in adults is presented.

zofran generic medication 2017-10-24

Serotonin is believed to be involved in the regulation of the gastric accommodation buy zofran reflex in man however which receptor subtype(s) are involved remains to be elucidated.

zofran 40 mg 2016-10-22

The efficacy of the serotonin antagonist ondansetron (GR 38032F) was evaluated in the prevention of nausea and vomiting induced by CMF chemotherapy in 29 breast cancer patients. At their first treatment course of CMF, all given IV on day 1 q 21 days, patients buy zofran were given oral antiemetic treatment as follows: ondansetron 8 mg, 2 h prior to CMF, repeated after 5 and 10 h the day of chemotherapy and then 8 mg tds for a minimum of 3 days to a maximum of 5 days following chemotherapy. At first course of CMF, complete protection from emesis and nausea was observed in 86.2% and 62% of patients, respectively. At subsequent CMF courses with ondansetron, complete control of emesis was observed in 80% of patients. Side effects were mild and no dystonic reactions were observed. Ondansetron represents an effective, safe, and easily administered outpatient regimen. The addition of a corticosteroid to ondansetron could further improve control of CMF-induced emesis.

zofran odt dose 2015-09-24

To evaluate the appearance of chemotherapy-induced nausea and vomiting, and to compare the Mestinon Overdose antiemetic efficacy of the triple combination of palonosetron, aprepitant and dexamethasone with that of our old regimen using first-generation 5-hydroxytryptamine 3-receptor antagonists and dexamethasone during gemcitabine and cisplatin chemotherapy in patients with advanced urothelial cancer.

zofran dose 2015-03-06

Stability and compatibility of ondansetron and granisetron with a variety of other agents used in the oncology setting generally are similar. Granisetron is compatible with all tested Y-site drugs; ondansetron Omnicef 100 Mg is not compatible with amsacrine or fluorouracil. Information for dolasetron is not as readily available; therefore, comparisons are difficult to make.

zofran children dosage 2015-08-20

Ondansetron (0.25 microM) enhanced CDDP (0-32 microM) cytotoxicity against EAC cells in vitro. In EAC-bearing mice ondansetron (0.2 mg/kg,ip) administered 1 h before CDDP (7 mg/kg, ip) did not modify the antitumor activity of CDDP. CDDP (7 mg/kg, ip) single treatment induced significant increases in blood urea nitrogen (2-fold) and serum creatinine (2.5-fold) and significant decreases in hematocrit (25%) and white blood cell count (39%) compared to saline treatment. Mice Glimepiride Amaryl Generic receiving ondansetron 1 h before CDDP showed no significant enhancement of CDDP-induced nephrotoxicity or myelosuppression compared to those pretreated with saline receiving the same dose of CDDP.

zofran odt generic 2015-07-05

The aim of the study was to evaluate the role of ramosetron for the prevention of chemoradiotherapy-induced nausea and vomiting (CRINV) in patients receiving upper Precose 25 Mg abdominal irradiation with concurrent 5-fluorouracil chemotherapy.

zofran 1 mg 2017-07-08

A total of 255 surveys following emetogenic chemotherapy with daunorubicin, cyclophosphamide, carmustine, and etoposide and cytarabine combined, as well as intrathecal therapy with methotrexate, hydrocortisone, and Aldactone Pill cytarabine, were analyzed. Analysis was performed on surveys of 149 courses without antiemetic therapy and 106 courses after 2 doses of ondansetron 0.15 mg/kg iv. The most emetogenic chemotherapy treatment was the etoposide/cytarabine combination (p < 0.05). Ondansetron completely protected patients (defined as no nausea or no vomiting) during most (> 50%) of the chemotherapy treatments, except for those in which cyclophosphamide was used. Ondansetron provided greater control of nausea and vomiting, a higher percentage of complete protection, and decreased the daily activity interference rating for carmustine and etoposide/cytarabine compared with courses of chemotherapy without antiemetics (p < 0.05). Two intravenous doses of ondansetron also provided durable antiemetic efficacy over time for the most emetogenic chemotherapy treatment (etoposide/cytarabine).

zofran normal dose 2015-02-13

OND-OPT Aricept Medication Class are able to realize ideal controlled drug release.

pediatric zofran dose 2016-07-13

Patients received intravenous (IV) melodopramide 0.25 mg/kg, IV on dansetron 0.15 mg/kg, or IV saline placebo after induction of standardized halothane, nitrous oxide, and oxygen anesthesia. Muscle relaxants and their antagonists were allowed. Patients received Propecia Name Brand postoperative analgesics as needed.

zofran reviews 2017-10-24

This analysis evaluated whether the antiemetic efficacy of the NK1 receptor antagonist aprepitant (EMEND trade mark, Merck, Whitehouse Station, NJ) plus standard antiemetics could be sustained for Vermox Alcohol up to six cycles of cisplatin-based chemotherapy.

zofran uses alcohol 2016-05-06

To determine if higher doses of oral ondansetron are associated with greater efficacy or side effects.

zofran normal dosage 2015-09-15

126 ASA physical status I and II patients undergoing outpatient plastic surgery with three or more risk factors for PONV.

zofran generic lawsuit 2016-11-30

Postoperative nausea and vomiting (PONV) is a multifactorial problem after general anesthesia. Despite antiemetic prophylaxis and improved anesthetic techniques, PONV still occurs frequently after craniotomies. P6 stimulation is described as an alternative method for preventing PONV. The primary aim of this study was to determine whether P6 acupressure with Sea-Band could reduce postoperative nausea after elective craniotomy. Secondary aims were to investigate whether the frequency of vomiting and the need for antiemetics could be reduced.

zofran medication pregnancy 2015-08-06

Drugs that enhance the action of serotonin (5-hydroxytrypamine, 5-HT), including several selective serotonin reuptake inhibitors (SSRIs), reduce susceptibility to seizure-induced respiratory arrest (S-IRA) that leads to death in the DBA/1 mouse model of sudden unexpected death in epilepsy (SUDEP). However, it is not clear if specific 5-HT receptors are important in the action of these drugs and whether the brain is the major site of action of these agents in this SUDEP model. The current study examined the actions of agents that affect the 5-HT3 receptor subtype on S-IRA and whether intracerebroventricular (ICV) microinjection of an SSRI would reduce S-IRA susceptibility in DBA/1 mice. The data indicate that systemic administration of SR 57227, a 5-HT3 agonist, was effective in blocking S-IRA in doses that did not block seizures, and the S-IRA blocking effect of the SSRI, fluoxetine, was abolished by coadministration of a 5-HT3 antagonist, ondansetron. Intracerebroventricular administration of fluoxetine in the present study was also able to block S-IRA without blocking seizures. These findings suggest that 5-HT3 receptors play an important role in the block of S-IRA by serotonergic agents, such as SSRIs, which is consistent with the abnormal expression of 5-HT3 receptors in the brainstem of DBA mice observed previously. Taken together, these data indicate that systemically administered serotonergic agents act, at least, in part, in the brain, to reduce S-IRA susceptibility in DBA/1 mice and that 5-HT3 receptors may be important to this effect.