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Responses of plasma oxytocin and arginine vasopressin to nausea induced by apomorphine and ipecacuanha.

Apomorphine, a centrally-acting emetic, was administered subcutaneously (50 micrograms/kg) to nine normal subjects (four male, five female; aged 22-36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24-49 years). In the normal subjects this stimulus caused nausea (and vomiting in seven of nine) with a latency of 9.5 +/- 0.9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0.9 +/- 0.2 pmol/l to 249 +/- 104 pmol/l at 15 min after the onset of symptoms; mean +/- SEM, P less than 0.01). There was a small but significant increase in plasma oxytocin (OXT) concentration (from 1.6 +/- 0.4 pmol/l to 6.2 +/- 3.4 pmol/l; P less than 0.05). Mean arterial pressure (MAP) fell slightly (from 87 +/- 1.9 mm Hg to 71 +/- 4.4 mm Hg; P less than 0.05) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 10.0 +/- 1.4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 +/- 4 mm Hg to 71 +/- 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22-36 years) six of whom also underwent apomorphine tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The responses of arginine vasopressin and adrenocorticotrophin to nausea induced by ipecacuanha.

Ipecacuanha syrup induces emesis by an early peripheral (gastric irritant) action and a later central effect at the chemoreceptor trigger zone (CTZ). We have studied the responses of plasma AVP, ACTH and ACTH-precursors to early and late ipecacuanha-induced nausea in nine healthy male subjects. Symptom severity was assessed using a linear analogue scale. All subjects reported 'early' nausea (N1) with a latency of 16 +/- 2 min (mean +/- SEM) and eight subjects vomited. Six subjects experienced recurrent nausea (N2) (latency 106 +/- 10.4 min) of whom five also vomited. The interval between the cessation of N1 and the onset of N2 was 55 +/- 10.8 min (range 25-80 min). The severity of nausea at the onset of N1 or N2 was similar but the AVP and ACTH responses were highly variable. Thus, while mean plasma AVP concentrations increased during both symptom periods, in three subjects during N1 and in three subjects during N2 plasma AVP concentrations did not rise above the normal range, despite marked symptoms. No clear pattern of AVP response to distinguish early peripheral from late central ipecacuanha-induced emesis was demonstrated. Whilst mean plasma ACTH concentrations increased during both N1 and N2 there were no changes in mean plasma ACTH-precursor concentrations. Analysis of pooled data for N1 and N2 demonstrated direct correlations between the nausea score and the peak incremental plasma responses of either AVP or ACTH and, despite the variability, peak incremental concentrations of AVP and of ACTH were also correlated. The data indicate that there is no difference in the AVP responses to peripherally or centrally stimulated ipecacuanha-induced nausea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

Effects of propofol on ipecacuanha-induced nausea and vomiting.

BACKGROUND: The purpose of this study was to evaluate if propofol has 5-HT3 antagonistic effects. Ipecacuanha is known to release serotonin (5-HT) in the gastrointestinal tract and therefore ipecacuanha syrup was used to induce nausea and vomiting. The 5-HT3 antagonist ondansetron was used as a control substance. METHOD: Ten healthy male volunteers (20-37 years) were studied on three occasions and were randomly allocated to receive a concomitant infusion of propofol (initial bolus 0.1 mg kg(-1) then 1 mg kg(-1)h(-1)), ondansetron (initial bolus 0.11 mg kg(-1) then 14 microg kg(-1)h(-1)) and placebo on either occasion. The infusions started 30 min before oral ingestion of 30 ml of ipecacuanha and continued until 150 min after the intake. The number of retchings was recorded and the intensity of nausea was estimated by the subjects on a visual analog scale. RESULTS: During the first 150 min after ingestion of ipecacuanha there were no retchings during the ondansetron infusion (P=0.01 vs placebo, P=0.02 vs propofol) and significantly fewer retchings during propofol infusion compared to placebo (P<0.02). There was no nausea during the ondansetron infusion (P<0.01 vs placebo and propofol) but the volunteers experienced nausea both during the placebo and propofol infusion (NS). CONCLUSION: This study in volunteers has shown that propofol reduces the intensity of retching after oral intake of ipecacuanha syrup. As ipecacuanha releases 5-hydroxytryptamine, it can be concluded that propofol may have a weak 5-HT3 antagonistic effect.

Adult↗

Betamethasone does not prevent nausea and vomiting induced by ipecacuanha.

BACKGROUND: Corticosteroids reduce the incidence of PONV but the mode of action is not known. The purpose of this study was to evaluate if betamethasone has serotonin (5-HT) antagonistic effects. Ipecacuanha is known to release serotonin and therefore it was used to induce nausea and vomiting. The 5-HT3 antagonist ondansetron was used as a control substance. METHODS: In a randomized, double-blind, cross-over, placebo-controlled study 10 healthy male and female volunteers (6 M/4F), mean age 19.5 (18-23) years, mean weight 69.7 (53-84) kg, were studied on three occasions separated by at least 1 week. They were randomly allocated to receive pretreatment with betamethasone 8 mg, ondansetron 8 mg, or normal saline 2 ml as placebo on each occasion, 15 min before oral ingestion of 30 ml of Ipecacuanha syrup. After ingestion of ipecacuanha, vomitings were recorded and the intensity of nausea was estimated with a visual analog scale during 2 h. RESULTS: During the first 2 h after ingestion of ipecacuanha nine of the 10 volunteers vomited both after betamethasone and placebo. No volunteer vomited after ondansetron (P < 0.01 vs. betamethasone and placebo). The max VAS for nausea was significantly higher after betamethasone and placebo compared to ondansetron (P < 0.01). There were no statistically significant differences of the max VAS for nausea between betamethasone and placebo. CONCLUSION: This study in volunteers has shown that betamethasone does not prevent nausea and vomiting induced by oral intake of ipecacuanha syrup. As ipecacuanha releases 5-hydroxytryptamin, it can be concluded that betamethasone does not have 5-HT3 antagonistic effects.

Adolescent↗