Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A majority of patients experience pruritus, nausea and/or emesis following epidural morphine administration post-cesarean section. Naloxone or diphenhydramine are commonly used to treat these side effects. Prevention or reduction in the incidence of side effects of epidural morphine is a clinical goal. The purpose of the study was to observe the efficacy of prophylactic administration of hydroxyzine on the incidence and severity of pruritus following the epidural administration of morphine in 40 patients who requested epidural morphine for postoperative pain relief. Group I (n = 20) received saline, while Group II (n = 20) received 50 mg of hydroxyzine ten minutes after the administration of 5 mg epidural morphine. Both solutions were administered by deep intramuscular injection in the thigh area. The results of this investigation demonstrated that hydroxyzine was efficacious in attenuating the incidence of severe pruritus.
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PMID:Epidural morphine pruritus reduction with hydroxyzine in parturients. 191 5

To evaluate the safety and possible efficacy of high-dose naloxone for the treatment of acute cerebral ischemia, 38 patients received a loading dose of 160 mg/m2 over 15 minutes followed by a 24-hour infusion at the rate of 80 mg/m2/hr. Nausea and/or vomiting were common side effects. Naloxone was discontinued in seven patients (because of hypotension in one, bradycardia and hypotension in two, myoclonus in one, focal seizures in two, and hypertension in one); all seven patients responded to treatment and no permanent sequelae to naloxone were noted. Twelve of the 38 patients showed early neurologic improvement (by completion of the naloxone loading dose). However, there was no correlation between such a loading dose response and clinical outcome at 3 months. Our experience suggests that naloxone is safe at the dose used, but data for efficacy are inconclusive.
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PMID:High-dose intravenous naloxone for the treatment of acute ischemic stroke. 233 51

In the first part of this study, we compared the effects of morphine and trimebutine, two opioid receptor agonists, on small intestinal motility and plasma motilin in dogs. Morphine (100 micrograms/kg iv for 10 min) induced first a typical vomiting myoelectric profile followed subsequently by a migrating electrical activity mimicking phase III of the migrating myoelectric complex; trimebutine (5 mg/kg iv for 10 min) initiated only a migrating phase III-like activity. Despite their different initial contractile effects, both agents induced a significant and similar rise in plasma motilin that preceded the beginning of the premature phase III. In the second portion of the study, naloxone, an opioid receptor antagonist, was infused to verify the influence of endogenous opiates on plasma motilin and on the migrating motor complex. Naloxone (2 mg/kg, then 0.5 mg.kg-1.h-1 iv) delayed significantly the cyclic recurrence of plasma motilin peak increases and of the phase IIIs. In some animals, where naloxone abolished the phase IIIs, the amplitude of the motilin peak increases was significantly diminished. These results suggest 1) that opioid administration increases plasma levels of motilin by a mechanism that is independent of the intestinal contractile activity, and 2) that endogenous opioids could be physiological inducers of plasma motilin increases in the conscious dog.
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PMID:Regulation of plasma motilin by opioids in the dog. 254 42

The role of opioid and histaminergic system in morphine induced emesis was investigated in dogs. Morphine (25 micrograms, icv) consistently evoked emesis with an average latency of 195 +/- 29 sec which was fully accounted for by an action on the chemoreceptor trigger zone (CTZ) as its ablation rendered animals refractory to vomiting. Intraventricular pretreatment with opioid antagonist naloxone, histamine H1 antagonist mepyramine and H2 antagonists metiamide and cimetidine afforded protection to icv morphine emesis. The CSF histamine concentration was significantly raised 5 min after icv morphine administration. The results suggest that both endogenous opioid and histamine are involved in morphine emesis. Naloxone in high doses (1600 micrograms, icv) elicited emesis which was not blocked by CTZ ablation confirming our earlier report.
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PMID:Role of endogenous opioids and histamine in morphine induced emesis. 260 22

This randomized investigation compared the efficacy of the conventional narcotic, meperidine, and a more potent and short-acting analgesic, fentanyl, during labor. One hundred five women with uncomplicated term pregnancies in active labor were randomly assigned to receive either intravenous fentanyl (50-100 micrograms every hour) or meperidine (25-50 mg every 2-3 hours) in a non-blinded manner. The analgesics were rated equivalent in efficacy. Maternal nausea, vomiting, and prolonged sedation occurred more frequently in the meperidine group. Naloxone use was significantly less in fentanyl- than in meperidine-exposed infants (one of 49 versus seven of 56; P less than .05). Neuroadaptive testing at approximately 2 hours and 24 hours postnatally revealed similar averaged scores in the two groups. Using the described intravenous dosing schedule, fentanyl was preferable to meperidine during labor because there was no prolonged maternal sedation or vomiting necessitating therapy and the requirement for neonatal naloxone was reduced.
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PMID:Randomized comparison of meperidine and fentanyl during labor. 279 37

To evaluate the role of endogenous opiates in chemo-therapy-induced nausea and vomiting, the narcotic-antagonist naloxone was administered to six pediatric patients receiving cancer chemotherapy. Naloxone was administered by continuous intravenous (i.v.) infusion after randomized, double-blind controlled assignment at a dose of 0, 10 or 40 micrograms/kg/h for 12 h. Each patient was studied for four consecutive and identical courses of chemotherapy (eight courses for each naloxone dose or 24 courses in all). A dose-related increase in nausea (nausea score 2.5 +/- 2.24, 3.83 +/- 2.73, and 5.75 +/- 2.86/12 h, p = 0.003), vomiting (emetic events 6.0 +/- 7.50, 8.08 +/- 6.71, and 10.3 +/- 8.91/12 h, p = 0.035), and patient aversion (course preference rank 1.5 +/- 0.45, 2.83 +/- 1.17, and 3.25 +/- 0.42/4 courses, p = 0.014) was observed. The infusion of naloxone in the absence of chemotherapy was without effect. These results support a role for endogenous opiates in regulating chemotherapy-induced nausea and vomiting, and further suggest that narcotic agents may be effective antiemetics in this setting.
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PMID:Increased nausea and vomiting induced by naloxone in patients receiving cancer chemotherapy. 305 43

Naloxone suppresses, but does not eliminate feeding in Siberian tigers. Naloxone administration paired with novel foods appeared to induce emesis.
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PMID:Naloxone induced suppression of feeding in tigers. 401 46

Although the incidence of obesity in the domesticated dog is high, few studies have investigated the regulation of food intake in this species. In the present study we investigated the response of the dog to a number of putative satiety agents including cholecystokinin (CCK), bombesin, calcitonin and naloxone. CCK significantly suppressed food intake during a scheduled fifteen minute meal in intact dogs and in dogs receiving total subdiaphragmatic vagotomies. Emesis occurred following injection of higher doses of CCK in most dogs. Bombesin and calcitonin reduced intake in both normal and vagotomized dogs, although higher doses of calcitonin were needed to significantly suppress feeding in vagotomized dogs compared with intact animals. Naloxone reduced feeding by as much as 60% in intact and vagotomized animals. Glucagon suppressed feeding in intact dogs, but not in vagotomized animals. Somatostatin and pancreatic polypeptide did not alter food intake. Thus the domesticated dog responds somewhat differently to some neuropeptides compared with the laboratory rat stressing the importance of examining the regulation of food intake across species.
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PMID:Peptidergic regulation of feeding in the dog (Canis familiaris). 614 23

1 The emetic action of Met-enkephalin, morphine and naloxone was studied following their administration into the cerebral ventricles of dogs through chronically implanted cannulae and the effect on the responses of ablating the chemorceptor trigger zone (CTZ) was investigated. The opiate antagonist, naloxone, was used to determine the role of enkephalin receptors in emetic responses.2 Administration of Met-enkephalin (1.0 mug/kg) into the IVth ventricle regularly evoked emesis with an average latency of 35 s. A dose of morphine (2.5 mug/kg) which was five times larger was required for a consistent emetic response when introduced into the lateral cerebral ventricle (i.c.v.) as compared to the dose required by the IVth ventricular route. The latency of emetic responses by the latter route of injection of morphine was shorter. This is in accord with an action of morphine on the emetic CTZ.3 After bilateral ablation of the CTZ, intraventricular injections of Met-enkephalin and morphine failed to produce emesis even when given in doses that were 5 to 10 times the dose which regularly elicited emesis in animals with intact CTZ. The emesis produced in dogs by intraventricular Met-enkephalin and morphine is thus fully accounted for by an action on the CTZ.4 Naloxone (i.c.v.) in doses up to 10.0 mug/kg did not cause emesis. However, higher doses of naloxone elicited dose-dependent emesis in dogs. The 100% emetic dose of naloxone was found to be 160 mug/kg and the latency of emesis was 180 s. Unlike Met-enkephalin and morphine, naloxone continued to elicit emesis in CTZ-ablated animals.5 Pretreatment with intraventricular naloxone (1 to 8 mug/kg) blocked the emetic responses induced by intraventricular Met-enkephalin and morphine but not that to apomorphine. The selective protective action of the opiate antagonist against Met-enkephalin and morphine supports the presence of enkephalin receptors in the emetic CTZ.
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PMID:Enkephalin receptors in the emetic chemoreceptor trigger zone of the dog. 626 66

This study determined the ED50 and ED90 of alfentanil for unconsciousness and anesthesia. A bolus of alfentanil was given to 28 healthy unpremedicated adults undergoing gynecologic or orthopedic procedures in one of four dosages: 100, 150, 200, or 250 micrograms/kg. Three indicators of induction were assessed 90 s later: eyelid reflex, response to verbal commands to breathe, and response to placement of a nasopharyngeal airway. Succinylcholine, given at 90 s, was followed by tracheal intubation 1 min later. From probit analysis, the ED50 and ED90 for loss of voice response were 92 and 111 micrograms/kg, respectively, and for loss of nasopharyngeal airway response, 111 and 169 micrograms/kg. A high incidence of chest wall rigidity (75%) and movements of the limbs (54%) or eyes (25%) was seen. There were statistically significant increases of the heart rate prior to stimulation and of both the heart rate (21% rise) and systolic blood pressure (10% rise) from control to the peak value following intubation. Differences between alfentanil doses were not significant. Naloxone was required in 36% of patients for end-tidal PCO2 greater than 48 mmHg at emergence from anesthesia; no patient required additional naloxone. Nausea or vomiting occurred in 39% of all subjects. Two patients recalled placement of the nasopharyngeal airway. We conclude that alfentanil is an anesthetic, and its ED50 (analogous to MAC of inhalational agents) is 111 micrograms/kg. The blood pressure and heart rate responses to laryngoscopy and intubation were modest after doses that allowed for extubation as early as 51 min after induction.
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PMID:ED50 of alfentanil for induction of anesthesia in unpremedicated young adults. 642 Nov 97


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