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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To study the serum level of ondansetron after oral administration of intravenous ondansetron, and test the palatability of the drug after being flavored.
The anti-emetic profile of the novel brain penetrant tachykinin NK1 receptor antagonist MK-0869 (L-754,030) 2-(R)-(1-(R)-(3,5-bis(trifluoromethyl)phenylethoxy)-3-(S)-(4-fluor o)phenyl-4-(3-oxo-1,2,4-triazol-5-yl)methylmorpholine and its water soluble prodrug, L-758,298, has been examined against emesis induced by cisplatin in ferrets. In a 4 h observation period, MK-0869 and L-758,298 (3 mg/kg i.v. or p.o.) inhibited the emetic response to cisplatin (10 mg/kg i.v.). The anti-emetic protection afforded by MK-0869 (0.1 mg/kg i.v.) was enhanced by combined treatment with either dexamethasone (20 mg/kg i.v.) or the 5-HT3 receptor antagonist ondansetron (0.1 mg/kg i.v.). In a model of acute and delayed emesis, ferrets were dosed with cisplatin (5 mg/kg i.p.) and the retching and vomiting response recorded for 72 h. Pretreatment with MK-0869 (4-16 mg/kg p.o.) dose-dependently inhibited the emetic response to cisplatin. Once daily treatment with MK-0869 (2 and 4 mg/kg p.o.) completely prevented retching and vomiting in all ferrets tested. Further when daily dosing began at 24 h after cisplatin injection, when the acute phase of emesis had already become established, MK-0869 (4 mg/kg p.o. at 24 and 48 h after cisplatin) prevented retching and vomiting in three out of four ferrets. These data show that MK-0869 and its prodrug, L-758,298, have good activity against cisplatin-induced emesis in ferrets and provided a basis for the clinical testing of these agents for the treatment of emesis associated with cancer chemotherapy.
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A random sample (N = 962) of Oncology Nursing Society members who designate themselves as practicing in the area of chemotherapy.
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Treatment results of advanced soft tissue sarcomas are still suboptimal. To evaluate the clinical effects of a combination therapy (FADIP) with Adriamycin (ADM), ifosfamide (IFO), cisplatin (DDP) plus continuous infusion of 5-fluorouracil (FU) as a synergistic factor for alkylating agents, a phase II study was initiated in patients with advanced soft tissue sarcomas of different histological subtypes. Fifty-six previously untreated patients with advanced soft tissue sarcomas of different histological subtypes (24 females, 31 males, median age 51.3 years, median Karnofsky performance status 80%) were included in this study. Treatment consisted of ADM 50 mg/m2 i.v. on day 1, IFO 4,000 mg/m2 i.v. on day 1, mesna 800 mg/m2 i.v. 3 x with 8-hour intervals on day 1 starting with IFO administration, FU 500 mg/m2 i.v. as 24-hour infusion on days 1 + 2, DDP 100 mg/m2 i.v. on day 2. This regimen was repeated every 4 weeks for at least 2 cycles. Major WHO grade III/IV hematological toxicity was observed in 35/56 patients. One toxic death due to severe neutropenia and fungal pneumonia occurred. Granulocyte colony-stimulating factor was administered in 8/35 neutropenic patients. Time to recovery was significantly reduced and no infectious complication was observed. WHO grade III/IV toxic diarrhea was observed in 8 patients requiring intravenous fluid replacement. WHO grade III/IV nausea occurred in 11 patients, 9/11 responded to symptomatic treatment with ondansetron alone. The overall response rate was 30.3%. The median duration of response (complete/partial response, CR/PR) was 18.1 months, the median progression-free interval was 4.5 months. The median survival time of all patients was 11.8 months, and 18.1 months in responding patients (CR/PR). Tumor-related pain was effectively reduced in 15/31 patients under treatment. FADIP produces comparable response rates to other standard treatment regimens in soft tissue sarcomas. Prolonged duration of response and median survival may be due to the use of continuous infusion of FU as a synergistic factor to alkylating agents. Granulocyte colony-stimulating factor is effective in reducing the otherwise observed high rate of WHO grade III/IV hematological toxicity with severe neutropenia.
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In the 24 hours after surgery, aprepitant 40 mg was more effective than ondansetron for all five endpoints evaluated: (1) no significant nausea (56.4% vs. 48.1%); (2) no nausea (39.6% vs. 33.1%); (3) no vomiting (86.7% vs. 72.4%); (4) no nausea and no vomiting (38.3% vs. 31.4%); and (5) no nausea, no vomiting, and no use of rescue (37.9% vs. 31.2%) (p < 0.035 for the odds ratio for each comparison). Numerically more patients receiving aprepitant 125 mg also achieved these endpoints compared with ondansetron.
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Neuropathic pain is a debilitating condition that is often resistant to common analgesics, such as opioids, but is sensitive to some antidepressants, an effect that seems to be mediated by spinal cord 5-HT3 receptors. Because the analgesic potential of monoamine oxidase-A (MAO-A) inhibitors is understudied, we evaluated the potential antinociceptive effect of the reversible MAO-A inhibitors moclobemide and 2-(3,4-dimethoxy-phenyl)-4,5-dihydro-1H-imidazole (2-DMPI) in a mouse neuropathic pain model induced by chronic constriction injury (CCI) of the sciatic nerve. Neuropathic mice showed a decreased mechanical paw withdrawal threshold (PWT) 7 days after lesion compared with the baseline PWT, characterizing the development of hyperalgesia. Moclobemide (100-300 μmol/kg, s.c.) and 2-DMPI (30-300 μmol/kg, s.c.) treatments were able to reverse the CCI-induced hyperalgesia, with 50% inhibitory dose (ID50) values of 39 (18-84) and 11 (4-33) μmol/kg, and maximum inhibition (Imax) values of 88±14 and 98±15%, respectively, at the 300 μmol/kg dose. In addition, we observed a significant increase in the MAO-A activity in the lumbar spinal cord of CCI-submitted mice compared with sham-operated animals. Furthermore, the antihyperalgesic effects of both 2-DMPI and moclobemide were largely reversed by intrathecal injection of the 5-HT3 receptor antagonist ondansetron (10 μg/site). These results suggest a possible involvement of MAO-A in the mechanisms of neuropathic pain and a potential utility of the reversible inhibitors of MAO-A in the development of new therapeutic approaches to treat it.
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This paper describes a multicentre, double-blind, parallel group study which compared ondansetron (0.15 mg/kg i.v. x 3) plus dexamethasone (20 mg i.v.) with metoclopramide (3 mg/kg i.v. x 2) plus dexamethasone (20 mg i.v.) and diphenhydramine (50 mg i.v.) for the prevention of cisplatin-induced emesis and nausea. Two hundred and eighty-nine consecutive patients receiving chemotherapy containing cisplatin at doses > or = 50 mg/m2 entered the study and 267 patients were evaluable for efficacy. The ondansetron regimen was significantly superior compared with the metoclopramide regimen in the control of acute emesis and nausea. Ondansetron plus dexamethasone provided complete protection against retching and vomiting in 79% of patients compared with 59% of patients given the metoclopramide combination (p < 0.002). Similarly ondansetron plus dexamethasone completely prevented nausea in 77% of patients, whereas the metoclopramide combination protected 66% of patients (p < 0.051). Success (no nausea and no emesis) was afforded to 69% of those patients given ondansetron plus dexamethasone as opposed to 50% of patients given the metoclopramide combination (p < 0.003). From day 2-4 all patients received the same anti-emetic regimen of oral metoclopramide and intramuscular dexamethasone. Significantly fewer patients who had received the ondansetron regimen on day 1 vomited on days 2 and 3 compared with those who had received the triple drug combination (84-86 and 68-71%, respectively, p < 0.006). Nausea was also better controlled in this group on day 2. On subsequent cisplatin cycles, the incidence of acute vomiting rose to 53% in those patients given the metoclopramide regimen, but remained low (26%) in the group treated with ondansetron plus dexamethasone. Patients receiving the metoclopramide regimen had significantly more sedation than patients receiving ondansetron plus dexamethasone (12 vs. 2%; p < 0.005). Extrapyramidal reactions were only observed in metoclopramide-treated patients (3%). The results of this study suggest that ondansetron plus dexamethasone is a more effective and better tolerated anti-emetic regimen compared with metoclopramide plus dexamethasone and diphenhydramine for the prevention of acute cisplatin-induced emesis.
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University affiliated, 280-bed pediatric hospital.
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Cochlear implants are now an acceptable therapeutic option for those patients with irreversible hearing loss and deaf-mutism. The surgery is time consuming and complicated. Hence, the technique of anaesthesia plays a crucial role in success of cochlear implant surgery. Cochlear implant patients have various types of syndromes which are important from anaesthetic as well as surgical point of view. Pre-implant preparation requires objective assessment of hearing, plain X-rays of skull and a CT scan of the temporal bone. Anaesthesia is required for objective assessment of hearing in children under five years of age, to obtain X-rays of skull, magnetic resonance imaging (MRI), CT scan, brain evoked response audiometry (BERA) testing and finally for cochlear implant surgery. Anaesthetic considerations include preoperative familiarisation with the patient and his family. Syndromal illnesses have specific anaesthetic significance such as presence of difficult airway or prolonged QT interval. Parental presence is highly desirable during induction of anaesthesia. Electro-surgical instruments especially monopolar ones, should not be used once the cochlear implant is in place.
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In the year under review there have been steady advances in anaesthesia. Premedication in children is best achieved with oral midazolam formulated in flavoured syrups, and the inhalational induction of anaesthesia may be accomplished using sevoflurane. Pain management of the most common surgical procedure performed in children, tonsillectomy/adenoidectomy, is still sub-optimal, but combinations of opioids and non-steroidal anti-inflammatory drugs are helpful. There are, however, some concerns regarding the possible increases in postoperative blood loss after tonsillectomy when non-steroidal anti-inflammatory drugs are used. Middle ear surgery leads to a high incidence of postoperative nausea and vomiting, and these are best managed by utilizing a total intravenous anaesthetic technique with propofol, the avoidance of nitrous oxide, and administration of dexamethasone and a 5-hydroxytryptamine receptor antagonist such as ondansetron.
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Wistar rats can develop a high preference for 3% alcohol after a period of forced alcohol exposure and 2 days of alcohol withdrawal. If these rats are selected at a medium (> or = 60%) and a high (> or = 85%) level of alcohol preference, it is possible to study the effects of various compounds on alcohol intake and alcohol preference in rats with two different levels of alcohol preference. With this procedure, it was demonstrated that the benzodiazepine chlordiazepoxide can reduce alcohol preference at doses > or = 10.0 mg/kg in the high alcohol preference group, by increasing the water consumption without affecting alcohol drinking. Chlordiazepoxide had no effects in the medium alcohol preference group. The 5-HT uptake inhibitors fluoxetine and citalopram reduced alcohol intake and alcohol preference in both the medium and the high alcohol preference groups by means of a reduction in consummatory behaviour. Both drugs clearly affected total fluid intake and body weight gain. The 5-HT1A agent buspirone reduced alcohol intake and alcohol preference in the group of medium alcohol preferring rats at doses between 0.0025 and 0.63 mg/kg. The drug did not change water drinking so that total fluid consumption diminished. At doses > or = 2.5 mg/kg buspirone, there was an increased alcohol consumption. Buspirone was without important effects on the high alcohol preferring rats. The 5-HT3 antagonist ondansetron reduced alcohol intake in both the medium and high alcohol preferring rats at doses between 0.01 and 0.16 mg/kg. The drug had no effects on alcohol preference and water consumption. At some doses, there was a reduction in total fluid intake. The 5-HT2/1C antagonist ritanserin reduced alcohol intake and alcohol preference at doses between 0.04 and 2.50, and 0.16 and 10.0 mg/kg in the medium and high alcohol preferring rats, respectively. Together with the decrease in alcohol consumption there was an increase in water drinking, leaving total fluid intake unaffected. The activity of ritanserin was less pronounced in the high as compared to the medium alcohol preference group. These results indicate that various serotonergic agents can affect alcohol intake and alcohol preference by different mechanisms of action.
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the results of our study suggest that MO protects ulcer formation by modulating 5-HT secretion through EC cell via 5-HT(3) receptors in gastrointestinal tract.
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Recently, a study on 5 patients [Holbrook et al.: J Allergy Clin Immunol 2013;132:1219-1220] documented the efficacy of the intravenous administration of ondansetron in children with acute symptoms due to food protein-induced enterocolitis syndrome (FPIES). We report on the experience at our institution using ondansetron during oral food challenge (OFC) in 5 children affected by FPIES. In all 5 cases, the use of intramuscular ondansetron led to a complete and rapid resolution of symptoms within 15 min. Intramuscular administration, without the need for intravenous access for an infusion or steroid administration, enables this therapy to be easily performed, even at home (i.e. out of a hospital setting). A home treatment with ondansetron cannot be considered as an alternative to a medical examination with eventual treatment in hospital, which is advised after any acute episode of FPIES. We consider ondansetron to be very useful in the management of acute FPIES. Further study is required to confirm its efficacy.
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In this randomized double-blind study, 131 patients were assigned to either group A (paracetamol+placebo), group B (paracetamol+pregabalin+placebo) or group C (paracetamol+pregabalin+dexamethasone). Pre-operatively, patients received either paracetamol 1000 mg, pregabalin 300 mg, dexamethasone 8 mg or placebo according to their allocation. Post-operative pain treatment included paracetamol 1000 mg 4× and ketobemidone 2.5 mg p.n. Ketobemidone consumption, pain scores [visual analogue scale (VAS)], nausea, sedation, dizziness, number of vomits and consumption of ondansetron were recorded 2, 4 and 24 h after the operation. P<0.05 was considered statistically significant.
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The severity of sickness in the first 5 days after cancer chemotherapy was compared in patients who had or had not received ondansetron 8 mg three times daily. Patients were divided into those having highly emetic chemotherapy, irrespective of gender and women having moderately emetic drugs. Ondansetron appeared to be more effective in the former group.
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To determine whether the addition of dexamethasone to ondansetron (OND + DEX) is a more effective antiemetic regimen than ondansetron (OND) alone in children receiving chemotherapy.
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Cannabis-based medications may be useful for treating refractory chemotherapy-induced nausea and vomiting. However, methodological limitations of the trials limit our conclusions and further research reflecting current chemotherapy regimens and newer anti-emetic drugs is likely to modify these conclusions.
The results show that outpatient laparoscopic cholecystectomy is safe and cost-effective in selected patients, and that the mock home setting provides a means of studying the safety of transition of care.
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Postoperative nausea, a common complication in patients receiving general anesthesia, was studied in this randomized investigation to compare the efficacy of 70% inhaled isopropyl alcohol and intravenous ondansetron. For the study, 100 healthy women, ASA physical status I or II, scheduled for outpatient gynecologic laparoscopic procedures randomly received 4 mg of intravenous ondansetron or isopropyl alcohol for the treatment of postoperative nausea. Nausea was measured on arrival to the postanesthesia care unit, at first complaint of nausea, every 5 minutes after initiation of therapy until nausea resolution, and every 15 minutes thereafter using a 0 to 10 verbal numerical rating scale. At 5, 10, and 15 minutes, the median verbal numerical rating scores between the ondansetron and alcohol groups were 6.00 and 3.00, 5.00 and 3.00, and 5.00 and 2.00, respectively (P = .002, .015, and .036, respectively). No statistically significant differences were found at any other time interval. Mean times from initiation of therapy to a 50% reduction in nausea between the ondansetron and alcohol groups were 6.3 minutes and 27.7 minutes, respectively (P = 0.022). Based on this study, it seems postoperative nausea can be resolved quicker using 70% inhaled isopropyl alcohol compared with intravenous ondansetron in women undergoing outpatient gynecologic laparoscopic procedures.
The selective serotonin re-uptake inhibitor (SSRI) citalopram decreases the synthesis of 5-hydroxytryptamine (5-HT) in the mouse brain in vivo. The underlying mechanism was studied by recording the accumulation of 5-hydroxytryptophan (5-HTP) in hypothalamus and hippocampus after inhibition of the aromatic amino acid decarboxylase activity with m-hydroxybenzylhydrazine (NSD 1015). Depletion of 5-HT with reserpine markedly reduced the citalopram-induced decrease of 5-HTP but not that evoked by the 5-HT1A receptor agonist 8-OH-DPAT, which indicates that the presence of endogenous 5-HT is necessary for full effect of citalopram. In contrast to the almost complete antagonism of the decrease in 5-HT synthesis induced by 8-OH-DPAT, the 5-HT1A receptor antagonist WAY-100,635 only slightly affected the citalopram-evoked decrease in 5-HT synthesis. Likewise, the 5-HT1B receptor antagonists NAS-181 and GR127935 only slightly antagonised the citalopram effect although they strongly inhibited the decrease in 5-HT synthesis induced by the 5-HT1B receptor agonist anpirtoline. Combined treatment with 5-HT1A and 5-HT1B receptor antagonists did not produce any additive antagonistic effect on the citalopram-induced decrease in 5-HT synthesis. The 5-HT2A/2C receptor antagonist ketanserin, the 5-HT3 receptor antagonist ondansetron and the 5-HT4 receptor antagonist RS-39604 had no effect on the citalopram-induced decrease in 5-HT synthesis. The same was found for several other non-selective 5-HT receptor antagonists, e.g. cyproheptadine, dihydroergotamine, methiothepin, methysergide, metergoline and mianserin. It is concluded that the citalopram-induced decrease in 5-HT synthesis differs in sensitivity from that mediated by 5-HT1A or 5-HT1B receptor agonists and citalopram also seems to require endogenous 5-HT for its full effect.
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 effects and mechanisms of intestinal electrical stimulation (IES) with long pulses on intestinal motility were investigated in conscious dogs. Eighteen dogs were equipped with serosal electrodes and an intestinal cannula in the small bowel. The first experiment was designed to study the effect of one-channel IES on intestinal motility and the extent of this effect. The second experiment was conducted to study the effect of IES on intestinal motility and the involvement of neural pathway. The IES with long pulses significantly inhibited intestinal motility. Intestinal motility of the entire measured segment (40-220 cm distal to the stimulation electrodes) was inhibited by 60-74% with the single-channel IES with long pulses. Hexamethonium, guanethidine, phentolamine, propranolol partially, but not N(omega)-nitro-L-arginine (L-NNA), ondansetron and naloxone prevented the inhibitory effect of IES on intestinal motility. We conclude that single-channel IES inhibits intestinal motility within a distance of at least 2 m. This inhibitory effect induced by IES with long pulses is mediated via sympathetic but not nitrergic, serotoninergic 5-HT(3) and opiate pathway.
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The study was carried out to compare the efficacy of ginger (Zingiber officinale) added to Ondansetron in preventing PONV after ambulatory surgery.
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Sixty patients who underwent surgery under general anesthesia for spinal fusion were randomly assigned to receive sevoflurane-nitrous oxide-oxygen (group SO, n = 20), sevoflurane-remifentanil-nitrous oxide-oxygen (group SR, n = 20), or propofol-remifentanil-oxygen (group PR, n = 20) in a double-blinded manner. All patients within 1 hour after induction received PCA (fentanyl 0.4 µg/kg/ml and ondansetron 16 mg) administered intravenously at a basal infusion rate of 1 ml/h, after being intravenously injected with a loading dose of fentanyl (1 µg/kg). Data for fentanyl requirement, verbal Numerical Rating Scale (NRS) pain score at rest, and presence of nausea or vomiting were collected at 1, 24, and 48 hours after surgery.
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Serotonin receptors are involved in the accelerating effect of erythromycin on gastric emptying. This effect seems to be enhanced by pre-treatment with octreotide, possibly as a result of the modification of the gastrointestinal hormonal environment.
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GC-7101 revealed a prokinetic effect through enhancing the contractile responses of ESMCs, tone increases, enhancing the carbarchol- or EFS-induced contractile responses of LES muscle strips, and the acceleration of GE and GIT. We have identified the significant potential of GC-7101 for the development of new prokinetic drugs through this study.
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The well established bowel cleansing method using a polyethylene glycol-based solution (Fordtran) is limited by the necessity of large volume intake, which proves difficult for many patients. Therefore, a new method using small volumes (2 x 90 ml) of oral sodium phosphate is employed more and more frequently. Its only disadvantage is the occurrence of considerable nausea or occasional vomiting in about 25% of patients. To ascertain whether nausea could be reduced, 426 patients were given an antiemetic (ondansetron, metoclopramide, cisapride) or placebo on a randomized, double-blind basis, one hour before sodium phosphate intake.
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Three hundred twenty-two patients who had been given > or = 50 mg/m2 of cisplatin were randomly assigned to receive, from days 2 to 4 after chemotherapy, oral ondansetron (8 mg twice daily) or oral metoclopramide (20 mg every 6 hours), both associated with intramuscular dexamethasone (8 mg twice on days 2 and 3, and 4 mg twice on day 4). Patients received the same intravenous prophylaxis for acute emesis: ondansetron 8 mg and dexamethasone 20 mg. Nausea and vomiting were assessed daily until day 6 after chemotherapy.
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Serotonin and serotoninergic drugs have significant effects on respiration, at many sites throughout the nervous system, and serotonin has been implicated in the pathogenesis of obstructive sleep apnea. Thus, understanding the serotoninergic mechanisms underlying respiratory control may help discover novel pharmacotherapies for sleep-disordered breathing. Ondansetron, a serotonin (5-HT) antagonist selective for the 5-HT3 receptor subtype has recently been shown to suppress sleep-related central apneas in rats, particularly in rapid-eye-movement (REM) sleep. To evaluate the potential of ondansetron in the treatment of obstructive sleep-disordered breathing, we have performed randomized trials of two doses of ondansetron (20 and 40 mg orally) and placebo (4 studies for each of the 3 conditions) in our animal model of obstructive sleep apnea, the English Bulldog. Ondansetron significantly reduced the respiratory disturbance index (RDI) in REM sleep from 24.15+/-4.85 events/hour at placebo to 11.01+/-1.56 events/hour with high dose treatment, n=4, p<0.05. In contrast, the effects of drug on the RDI in non-rapid-eye-movement (NREM) sleep (5.23+/-1.30 events/hour, placebo; 4.31+/-1.36, with 20 mg ondansetron and 2.89+/-1.30 with 40 mg ondansetron, n=4) were not significant. Ondansetron, however, had no effect on either sleep efficiency or sleep architecture, and there were no effects on either oxyhemoglobin saturation nadirs or on the sleep time with saturations <90%. Although a trend towards reduction in the latter measure of oxygenation was seen at the higher dose of ondansetron. These data suggest a therapeutic potential for ondansetron in obstructive sleep-disordered breathing, particularly REM sleep apnea.
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