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The Bötzinger complex as the pattern generator for retching and vomiting in the dog.

To clarify the location of the pattern generator for the emetic act, the bulb was systematically stimulated and partially cut in decerebrate, paralyzed dogs. Stimulation of the following bulbar structures elicited the activities which could be recognized as retching and vomiting in the following muscle nerves. The bulbar structures were: the intra-bulbar bundle of the vagal afferents, the solitary tract and the medial subdivision of its nucleus (NTS), the area postrema, the commissural nucleus, the raphe area at the obex level, and the longitudinal reticular column which consists of 3 areas--the area between the caudal parts of the solitary complex (SC) and the nucleus ambiguus, the area ventromedial to the rostral part of the nucleus and the area dorsomedial to the retrofacial nucleus (RFN) which may correspond to the Bötzinger complex (BOT). The muscle nerves were: the phrenic branches to the dome and hiatal parts of the diaphragm, the abdominal muscle nerve, the pharyngo-esophageal branch of the vagus nerve, the mylohyoid muscle nerve, and the recurrent nerve branches to the adductors and abductor of the glottis. Emetic responses to stimulation of the vagal ventral trunk and the rostral SC still remained after cutting of the bilateral SCs at about 1 mm rostral to the obex, but disappeared after cutting at about 3.5 mm rostral to the obex. After the rostral cuts, stimulation of the SC part caudal to the cuts and the reticular column still induced the emetic act. Emetic responses to stimulation of the caudal SC remained after transection of the bulb at the rostral end of the RFN, but disappeared after transection at its caudal end or after partial cutting of the caudal BOT. The following hypothesis was proposed from these results. Emetic vagal afferents enter the rostral bulb, then descend through the SC to the area subpostrema. Subpostrema neurons project through the reticular column to the pattern generator of the emetic act in the BOT and activate it.

Animals↗

Cisplatin-induced early and delayed emesis in the pigeon.

1. Intravenously injected cisplatin at a dose of 4 mg kg(-1) induced early and delayed emesis in all pigeons without occurrence of lethality during a 72 h observation period. The early emetic response occurred with a latency of 81.3+/-8.0 min (n=15) and reached a peak at 2 - 3 h, and decreased gradually within 8 h after injection. Then the delayed emetic response, whose peak was found between 10 to 23 h, lasted up to 48 h. The emetic response markedly declined after 48 h. 2. Reserpine markedly reduced monoamine levels in both brain and intestine and completely abolished the early and delayed emesis. Dexamethasone markedly reduced not only the early but also the delayed emetic responses. p-Chlorophenylalanine decreased the level of serotonin in brain and intestine without affecting noradrenaline and dopamine and partly reduced the early emetic response, but did not affect delayed emesis. 3. Bilateral vagotomy prolonged the latency time to the onset of early emesis, and reduced the emetic responses in both the early and delayed phases. 4. The above results suggest that the cisplatin-induced early emesis in the pigeon is partially mediated via the vagal nerve and reserpine-sensitive monoaminergic systems including the serotonergic system; the delayed emesis is associated with monoaminergic but not the serotonergic systems.

Adrenergic Uptake Inhibitors↗

Cannabinoids inhibit emesis through CB1 receptors in the brainstem of the ferret.

BACKGROUND & AIMS: Marijuana and other cannabinoids are effective anti-emetics. Despite ongoing controversy over their usage, the receptor distribution and the site of the anti-emetic action of these compounds are not known. Our aim was to investigate whether the cannabinoid 1 receptor (CB1r) and endocannabinoids play a role in the anti-emetic action of cannabinoids. METHODS: Ferrets were given an emetic stimulus and the number of episodes of retching and vomiting were observed after administration of CB1r agonists and a CB1r antagonist. CB1r and fatty acid amide hydrolase (FAAH), which degrades endocannabinoids, were localized by immunohistochemistry. RESULTS: CB1r and FAAH were localized in the dorsal vagal complex, consisting of the area postrema, nucleus of the solitary tract, and the dorsal motor nucleus of the vagus in the brainstem. CB1r was found in the myenteric plexus of the stomach and duodenum. Activation of CB1r by the agonists (delta)(9)-tetrahydrocannabinol, WIN 55,212-2, and methanandamide inhibited emesis and their action was reversed by a selective CB1r antagonist, which alone had no effect, but potentiated vomiting in response to an emetic stimulus. CONCLUSIONS: CB1r mediates the anti-emetic action of cannabinoids in the dorsal vagal complex. Endocannabinoids are a novel neuroregulatory system involved in the control of emesis.

Animals↗

Biochemical and mutational analysis of the histidine residues of staphylococcal enterotoxin A.

The goal of this study was to examine the role of histidine residues in the biological activities of staphylococcal enterotoxin A (SEA). Carboxymethylated SEA was unable to stimulate murine T-cell proliferation but was resistant to monkey stomach lavage fluid degradation, suggesting that native conformation was intact. Site-directed mutagenesis of the histidine residues of SEA was subsequently performed. SEA-H44A (SEA with histidine 44 replaced with alanine), SEA-H44D, SEA-H50A, SEA-H50D, SEA-H114A, SEA-H114D, SEA-H187A, and SEA-H187D retained superantigen and emetic activities, whereas SEA-H225A and SEA-H225D were defective in the ability to stimulate T-cell proliferation. These mutants were unable to compete with SEA for binding to Raji cells, suggesting that the defect in SEA-H225A and SEA-H225D is due to impaired major histocompatibility complex class II binding. SEA-H225D provoked an emetic response in monkeys only if fed at high doses, while SEA-H225A did not provoke an emetic response at low or high doses. In comparison, SEA-H61A and SEA-H61D were defective in emetic activity but not in the ability to stimulate murine T-cell proliferation. Overall, these studies show that the carboxy-terminal histidine at residue position 225 of SEA is important for both the superantigen and emetic activities of this enterotoxin. Histidine 61 appears to be important for emetic activity but not for superantigen activity, consistent with the hypothesis that the two activities are separable in staphylococcal enterotoxins.

Animals↗

Some new aspects on emesis gravidarum. Relations to clinical data, serum electrolytes, total protein and creatinine.

Although nausea and vomiting in early pregnancy is extremely common, very little information on the cause and course of this disorder is available in the literature. A prospective laboratory and clinical study of 102 consecutive healthy pregnant women was undertaken to evaluate nausea and vomiting in relation to clinical data, serum electrolytes, creatinine, total protein and hemoglobin. Multigravidae suffered from emesis gravidarum at a higher rate than did primigravidae. The frequency of emesis was especially high in women with short intergestational intervals. During pregnancy there was a decline in systolic blood pressure only in non-emetic women. The diastolic blood pressure in late pregnancy was significantly higher in emetic women than in non-emetic subjects. All laboratory values were within normal ranges. However, major changes occurred during pregnancy but some alterations were noted only in the emetic pregnancy. A different response to the hormonal situation is suggested to explain the dissimilarities between the emetic and non-emetic pregnancy.

Adult↗

Randomized double-blind, placebo-controlled evaluation of oral ondansetron in the prevention of nausea and vomiting associated with fractionated total-body irradiation.

PURPOSE: To evaluate oral ondansetron in the prevention of total-body irradiation (TBI)-induced nausea and vomiting. METHODS: Twenty patients who received 4 days of TBI as part of their preparative regimen before bone marrow transplantation were randomized to receive either 8-mg oral doses of ondansetron or placebo. Administration of drug was double-blinded. Initial rescue therapy consisted of intravenous (i.v.) ondansetron 0.15 mg/kg following two or more emetic episodes between successive fractions of TBI or five total emetic episodes during the 4 days of therapy. If, after receipt of i.v. ondansetron, patients had two or more emetic episodes between fractions of TBI or five total emetic episodes, additional antiemetics were administered. RESULTS: Patients who received oral ondansetron had significantly fewer emetic episodes compared with those who received placebo (P = .005) over the entire 4-day study period. Oral ondansetron was also significantly superior to placebo with respect to the time of onset of emesis or rescue (P = .003). Six of 10 patients treated with oral ondansetron completed the study without additional antiemetic therapy, while none of 10 patients who received placebo completed the study without rescue antiemetic therapy. Six placebo patients who received initial rescue therapy with i.v. ondansetron required no additional antiemetics. No relationships were apparent between peak ondansetron concentration (Cmax) or area under the concentration versus time curve (AUC) and number of emetic episodes. CONCLUSION: Oral ondansetron is an effective therapy for the prevention of emesis induced by TBI.

Administration, Oral↗

American Society of Clinical Oncology guideline for antiemetics in oncology: update 2006.

PURPOSE: To update the 1999 American Society of Clinical Oncology guideline for antiemetics in oncology. UPDATE METHODOLOGY: The Update Committee completed a review and analysis of data published from 1998 thru February 2006. The literature review focused on published randomized controlled trials, and systematic reviews and meta-analyses of published phase II and phase III randomized controlled trials. RECOMMENDATIONS: The three-drug combination of a 5-hydroxytryptamine-3 (5-HT(3)) serotonin receptor antagonist, dexamethasone, and aprepitant is recommended before chemotherapy of high emetic risk. For persons receiving chemotherapy of high emetic risk, there is no group of patients for whom agents of lower therapeutic index are appropriate first-choice antiemetics. These agents should be reserved for patients intolerant of or refractory to 5-HT3 serotonin receptor antagonists, neurokinin-1 receptor antagonists, and dexamethasone. The three-drug combination of a 5-HT3 receptor serotonin antagonist, dexamethasone, and aprepitant is recommended for patients receiving an anthracycline and cyclophosphamide. For patients receiving other chemotherapy of moderate emetic risk, the Update Committee continues to recommend the two-drug combination of a 5-HT3 receptor serotonin antagonist and dexamethasone. In all patients receiving cisplatin and all other agents of high emetic risk, the two-drug combination of dexamethasone and aprepitant is recommended for the prevention of delayed emesis. The Update Committee no longer recommends the combination of a 5-HT3 serotonin receptor antagonist and dexamethasone for the prevention of delayed emesis after chemotherapeutic agents of high emetic risk. CONCLUSION The Update Committee recommends that clinicians administer antiemetics while considering patients' emetic risk categories and other characteristics.

Antiemetics↗

Dexamethasone has a central antiemetic mechanism in decerebrated cats.

Dexamethasone is an effective antiemetic drug, but its mechanism of action is unclear. We designed this study to investigate the direct antiemetic action of dexamethasone in the medulla of cats. By using an oscillographic vomiting model, decerebrated cats received microinjections of dexamethasone 100 nL (1 microg, n = 7; 0.1 microg, n = 7) into the bilateral nuclei tractus solitarii, which led to a significant prolongation of the latency (1 microg, 6.4 +/- 1.1 min versus 28.2 +/- 4.9 min, P < 0.05; 0.1 microg, 6.7 +/- 1.1 min versus 27.1 +/- 5.0 min, P < 0.05) of the first emetic episode and significantly decreased the frequency of emetic episodes (1 microg, 2.7 +/- 0.8 versus 0.1 +/- 0.4, P < 0.05; 0.1 microg, 2.9 +/- 0.9 versus 0.3 +/- 0.5, P < 0.05) induced by xylazine. Pretreatment with mifepristone, a glucocorticoid receptor antagonist, blocked the antiemetic effect of dexamethasone in the bilateral nuclei tractus solitarii. However, microinjection of dexamethasone into the unilateral nucleus tractus solitarius alone did not alter the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. Local application of dexamethasone into the area postrema had no effect on the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. These results suggest that dexamethasone exerts its central antiemetic action through an activation of the glucocorticoid receptors in the bilateral nuclei tractus solitarii in the medulla.

Animals↗

[Examination of toxin production from environmental Bacillus cereus and Bacillus thuringiensis].

Emetic toxin- and entero toxin-producing activities were examined for 524 strains of Bacillus cereus and 90 strains of Bacillus thuringiensis to determine the distribution and contamination in natural environment, including foods, vegetable, soil and etc. Emetic toxin was assayed by the production of acid from HEp-2 cells induced by the culture supernatants of Bacillus, which was developed as an improved method for the detection of B. cereus heat-stable emetic-toxin by us. In the 524 strains of B. cereus tested, 11 out of 60 strains obtained from bean paste and 5 out of 20 strains obtained from peach produced emetic toxin which was detected by the HEp-2 cell method. All these emetic toxin-producing isolate strains were classified into H1 serotype. The 90 strains of B. thuringiensis did not produce emetic toxin, but the 47 strains produced entero toxin.

Bacillus cereus↗

5-HT3 receptor antagonists ameliorate emesis in the ferret evoked by neutron or proton radiation.

BACKGROUND: Nausea and vomiting produced by sub-lethal doses of X- or gamma-rays can be ameliorated by serotonin subtype-three (5-hydroxytryptamine; 5-HT3) receptor antagonists. The effectiveness of these anti-emetics on blocking the emetic responses induced by fission neutron or proton radiation exposure was evaluated in the ferret animal model. HYPOTHESIS: 5-HT3 receptor antagonists or bilateral vagotomy will ameliorate that emesis evoked by fission neutrons or protons. METHODS: Groups of ferrets were exposed to whole-body or head-shielded radiations of varying qualities: fission spectrum neutons, high-energy protons, or gamma-rays. Prior to that exposure, some groups were either vagotomized or received subcutaneous (s.c.) or oral (p.o.) treatment with various doses of the 5-HT3 receptor antagonist antiemetics eusatron and ondansetron. RESULTS: We demonstrated that both eusatron and ondansetron effectively abolished the emesis normally induced by 2-Gy doses of either 60Co gamma or neutron:gamma, mixed-field irradiation, the latter with a neutron-to-total dose ratio (Dn/Dt) of 0.9+/-2% (%SD). Different routes of delivery of the anti-emetics yielded different degrees of inhibition of the emetic responses; p.o. treatment was less efficacious than s.c. treatment for the emesis to fission neutrons. Eusatron was significantly more effective than ondansetron on a mg x kg(-1) basis. Bilateral vagotomy also attenuated or abolished the emetic responses to the mixed-field neutron exposures. Furthermore, emesis induced by exposure to 2.5 Gy of 200-MeV protons was effectively abolished by ondansetron. CONCLUSION: These results are consistent with the concept that similar physiological and pharmacological mechanisms underlie the emetic responses to different qualities of radiation.

Administration, Oral↗

[Examination of inhibitory effect, safety and usefulness of SN-307 (ondansetron) administered orally once daily for 3-5 consecutive days on nausea and emesis associated with non-platinum anti-cancer drugs].

We examined the anti-emetic effect, safety and usefulness of ondansetron hydrochloride, a selective 5-HT3 receptor antagonist, given orally once daily at the dosage of 4 mg, for 3 to 5 consecutive days to patients with nausea and emesis induced by non-platinum anti-cancer drugs such as cyclophosphamide, doxorubicin and carboplatin. Out of 84 cases where anti-emetic effects were evaluated, numbers of cases assessed as excellent and good were 36 (83.3%) and 34 (40.5%), respectively, the efficacy rate being 83.3% (70/84). Side effects, such as moderate constipation (3 cases) and mild headache (3 cases), were observed in 8/85 cases (9.4%). Abnormalities in clinical laboratory findings including elevation of hepatic function and uricacid values and increase in eosinocyte counts, were observed in 3/85 cases (3.5%). As to overall safety, 78/85 cases (91.8%) were evaluated as having no problem in safety, and 7/85 cases (8.2%), as having minor problem in safety. As to clinical usefulness based on anti-emetic effect and overall safety, out of 79 cases the drug was assessed as very useful in 29 cases (36.7%) and useful in 35 cases (44.3%), the rate of "useful" or above being 81.0% (64/79). Furthermore, when ondansetron was administered in 3 courses of chemotherapy, though the number of patients was small, it was shown that anti-emetic effect of ondansetron did not decline and no problem in safety was observed. From the above, ondansetron which exerted adequate anti-emetic effect in 4 mg once daily doses was considered as a useful and safe anti-emetic in treatment of nausea and emesis associated with cancer chemotherapy.

Administration, Oral↗

Effect of macular ablation on frequency and latency of motion-induced emesis in the squirrel monkey.

Three previously motion-emetic sensitive squirrel monkeys were rendered refractory to a standard motion-emetic regimen by a two-stage utriculosacculectomy procedure which preserved the cristae ampullares of semicircular canals. Three non-operated control squirrel monkeys tested on the same motion-emetic regimen time schedule as the operated animals remained motion-emetic sensitive with regard to incidence, frequency, and latency of motion-induced emetic responses. Following a sham surgical procedure (stapedectomy) performed on two of the latter animals and one additional new animal, the emetic incidence decreased from 100% to 89%, but the frequency and latency were not altered significantly.

Acoustic Maculae↗

Ondansetron against metoclopramide/dexamethasone--a comparative study.

This trial was carried out in Hospital Kuala Lumpur. Fifty-two patients who were scheduled to receive their first or subsequent courses of cancer chemotherapy with single dose cisplatinum containing chemotherapy regimens were evaluated. Thirty-four patients were given ondansetron in one group while 18 in the other group received metoclopramide with dexamethasone. The response to treatment was categorised as complete (0 emetic episode), major (1 or 2 emetic episodes), minor (3 to 5 emetic episodes) or failure (> 5 emetic episodes or rescue medication). Among the 52 patients, a complete or major control (0 to 2 emetic episodes) was achieved in 23/34 patients (68%) from the ondansetron group and in 3/18 patients (17%) from the metoclopramide with dexamethasone group (p < 0.002) on day 1. Similarly, the control of nausea was greater in the ondansetron group compared with the metoclopramide with dexamethasone group (p < 0.0009) on day 1. Two patients were excluded (dropped out) after day one from each of the two study groups due to excessive vomiting subsequent to cisplatinum therapy. From days 2 to 6, there was a trend in favour of ondansetron. Both treatments were well tolerated. The results of this trial show that in the prophylaxis of nausea and vomiting induced by cisplatinum containing chemotherapy, the efficacy of ondansetron is superior to that of a standard anti-emetic combination, metoclopramide with dexamethasone.

Adult↗

The area postrema and vomiting.

The area postrema (AP) has been implicated as a chemoreceptor trigger zone for vomiting (emesis) for over 40 years. The AP is located on the dorsal surface of the medulla oblongata at the caudal end of the fourth ventricle. It is one of the so-called circumventricular organs that serve as an interface between the brain parenchyma and the cerebrospinal fluid (CSF)-containing ventricles. The AP lacks a specific blood-brain diffusion barrier to large polar molecules (i.e., a "blood-brain barrier") and is thus anatomically positioned to detect emetic toxins in the blood as well as in the CSF. The AP along with the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus makes up the so-called dorsal vagal complex, which is the major termination site of vagal afferent nerve fibers. Lesions of the AP prevent vomiting in response to most, but not all, emetic drugs. However, the AP is not essential for vomiting induced by motion or by activation of vagal nerve afferents. The role of the AP in radiation-induced vomiting remains controversial. Electrophysiological studies have reported that neurons in the AP increase their firing in response to emetic drugs. Similarly, studies using the 2-deoxyglucose uptake and c-fos expression techniques have shown that the AP is excited by systemic administration of emetic drugs. Activation of the AP probably leads to nausea and vomiting through its projection to the neighboring NTS. The NTS may serve as the beginning of a final common pathway by which different emetic inputs trigger vomiting.

Animals↗

Suncus murinus: a new experimental model in emesis research.

Effects of various emetic and antiemetic drugs were studied using Suncus murinus for its potential use as an experimental model in emetic research. Subcutaneous injection of nicotine bitartrate (10-15 mg/kg), veratrine sulfate (0.5-1.0 mg/kg), emetine dihydrochloride (40-80 mg/kg) and oral administration of copper sulfate (20-100 mg/kg) caused dose-dependent emesis in suncus. The ED50 of nicotine, veratrine, emetine and copper sulfate were 7.9, 0.4, 47.6 and 21.4 mg/kg, respectively. However, subcutaneously injected apomorphine hydrochloride (0.1-100 mg/kg), digitoxin (0.5-1.0 mg/kg) and orally administered emetine dihydrochloride (10-80 mg/kg) did not induce the vomiting. Chlorpromazine and promethazine decreased the emetic effect of nicotine, veratrine and copper sulfate, but scopolamine hydrobromide was not effective. These results indicate that the Suncus murinus is sensitive to various emetic and antiemetic drugs and can be used as a new experimental animal model for the emesis. Emetic behavior of suncus was discussed in comparison with other animals.

Animals↗

Comparison of the antiemetic effects of a 5-HT1A agonist, LY228729, and 5-HT3 antagonists in the pigeon.

Vomiting may be induced by a variety of agents such as drugs, oncolytics, and provocative motion, as well as being conditioned to occur to environmental stimuli. Such emesis has recently been shown to be blocked by agonists at the 5-HT1A subtype of serotonin receptor. The antiemetic effects of LY228729 [(-)-4-(dipropylamine)-1,3,4,5-tetrahydrobenz-(c,d)indole-6- carboxamide], a 5-HT1A receptor agonist, were tested and compared to the antiemetic effects of the 5-HT3 receptor antagonists ondansetron, tropisetron, and MDL 72222 (3-tropanyl-3,5-dichlorobenzoate). The emetic stimuli tested are known to be blocked by 5-HT3 antagonists in species other than the pigeon. In the pigeon, LY228729 totally abolished vomiting induced by fully emetic doses of cisplatin (10 mg/kg), ipecac (3 ml/kg), emetine (10 mg/kg), and a 5-HT3 agonist, m-(chlorophenyl)-biguanide (1.25 mg/kg). MDL 72222 blocked ipecac-induced vomiting in a dose-related manner and was partially effective in attenuating cisplatin-induced emesis. Ondansetron and tropisetron were partially effective in blocking emetine- and mCPBG-induced vomiting. Ondansetron exhibited an intrinsic emetic response that could not be blocked by MDL 7222, but which was eliminated by LY228729. It was concluded that 5-HT1A agonists are more effective in the pigeon than are 5-HT3 antagonists against these types of emetic stimuli. These results broaden the range of emetic stimuli that are blocked by 5-HT1A agonists in the pigeon.

Animals↗

The potent emetogenic effects of the endocannabinoid, 2-AG (2-arachidonoylglycerol) are blocked by delta(9)-tetrahydrocannabinol and other cannnabinoids.

Cannabinoids, including the endogenous cannabinoid or endocannabinoid, anandamide, modulate several gastrointestinal functions. To date, the gastrointestinal effects of the second putative endocannabinoid 2-arachidonoylglycerol (2-AG) have not been studied. In the present study using a shrew (Cryptotis parva) emetic model, 2-AG (0.25-10 mg/kg, i.p.) potently and dose-dependently increased vomiting frequency (ED(50) = 1.13 mg/kg) and the number of animals vomiting (ED(50) = 0.48 mg/kg). In contrast, neither anandamide (2.5-20 mg/kg) nor methanandamide (5-10 mg/kg) induced a dose-dependent emetogenic response, but both could partially block the induced emetic effects. Delta(9)-Tetrahydrocannabinol and its synthetic analogs reduced 2-AG-induced vomiting with the rank order potency: CP 55,940 > WIN 55,212-2 > Delta(9)-tetrahydrocannabinol. The nonpsychoactive cannabinoid, cannabidiol, was inactive. Nonemetic doses of SR 141716A (1-5 mg/kg) also blocked 2-AG-induced vomiting. The 2-AG metabolite arachidonic acid also caused vomiting. Indomethacin, a cyclooxygenase inhibitor, blocked the emetogenic effects of both arachidonic acid and 2-AG. CP 55,940 also blocked the emetic effects of arachidonic acid. 2-AG (0.25-10 mg/kg) reduced spontaneous locomotor activity (ED(50) = 11 mg/kg) and rearing frequency (ED(50) = 4.3 mg/kg) in the shrew, whereas such doses of both anandamide and methanandamide had no effect on locomotor parameters. The present study indicates that: 1) 2-AG is an efficacious endogenous emetogenic cannabinoid involved in vomiting circuits, 2) the emetic action of 2-AG and the antiemetic effects of tested cannabinoids are mediated via CB(1) receptors, and 3) the emetic effects of 2-AG occur in lower doses relative to its locomotor suppressant actions.

Animals↗

Inconsistency of prognostic factors for post-chemotherapy nausea and vomiting.

A number of prognostic factors have been reported to influence the probability of developing nausea and vomiting after cytotoxic chemotherapy. This study used data collected in four randomized anti-emetic trials conducted by the Clinical Trials Group of the National Cancer Institute of Canada (NCIC-CTG) to assess the consistency of the effects of these prognostic factors. A total of 582 patients, all of whom had received moderately emetogenic chemotherapy for the first time, but who were assigned to different anti-emetics, were included in the analysis. The major findings was that the probability of post-chemotherapy nausea and vomiting was much more strongly influenced by the type of chemotherapy given and the type of anti-emetic used than by patient (e.g., age, gender) or environmental (e.g., treatment location, time of administration) characteristics. Further, patient-related factors had different, and sometimes opposite, effects in different anti-emetic and chemotherapy subgroups. Finally, the relative potency of anti-emetics appeared to vary with chemotherapy regimens. Implications of these findings for future studies are discussed.

Antiemetics↗