Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1998
Clinical TrialGynecologic laparoscopic surgery is not associated with an increase of serotonin metabolites excretion.
Gynecologic laparoscopic surgery is associated with a high incidence of postoperative nausea and vomiting (PONV). The specific antagonists of the 5-hydroxytryptamine-3 (5-HT3) receptor have been progressively introduced in anesthesiology to prevent or treat PONV. Although a large increase of serotonin has been documented after cisplatin treatment, the link between serotonin and PONV in surgery/anesthesiology is unknown. In a prospective study, we compared the excretion of the serotonin metabolite 5-hydroxyindoacetic acid (5-HIAA) in 40 women undergoing either gynecologic laparoscopic surgery (laparoscopy group) or traditional open laparotomy surgery (laparotomy group). Premedication, anesthetic technique, and postoperative pain treatment were standardized. The excretion of 5-H IAA corrected to creatinine was measured in all patients immediately after the induction of anesthesia and was repeated regularly until 9 h after induction. The excretion of 5-HIAA/creatinine was similar in the two groups; no increase was observed in either group. The incidence of nausea and vomiting was 40% and 35%, respectively, in the laparoscopy group versus 60% and 15%, respectively, in the laparotomy group (not significantly different). The excretion of 5-HIAA/creatinine was comparable in patients of both groups among those who vomited and those who did not. We conclude that the creation of a pneumoperitoneum during gynecologic laparoscopic surgery is not associated with an increase of 5-HIAA excretion. PONV after gynecologic laparoscopic surgery is not explained by an increase of serotonin secretion. ⋯ The mechanism leading to the high incidence of postoperative nausea and vomiting after gynecologic laparoscopic surgery is unknown. The excretion of the serotonin metabolite 5-hydroxyindoacetic acid did not increase during the creation of the pneumoperitoneum and the first 9 h postoperatively. Increase of serotonin secretion from the gut may not explain postoperative nausea and vomiting associated with this surgery.
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Anesthesia and analgesia · Nov 1998
Influence of nitric oxide on vascular, metabolic, and contractile responses to dobutamine in in situ canine hearts.
The left anterior descending coronary arteries of 30 anesthetized, open-chest dogs were perfused via an extracorporeal circuit. Coronary blood flow (CBF), myocardial oxygen consumption (MVO2), and segmental shortening (SS) were measured. Studies were performed with coronary perfusion pressure (CPP) or CBF constant. With CPP constant, effects of intracoronary (IC) infusions of dobutamine (2.5, 5.0, or 10.0 microg/min) were evaluated alone (control) and after inhibition of nitric oxide (NO) synthase with NG-nitro-L-arginine methyl ester (L-NAME). With CBF constant, a NO donor (sodium nitroprusside [SNP] 80 microg/min IC) or nitroglycerin [NTG] 40 microg/min IC) or a releaser of endogenous NO (acetylcholine [ACh]; 20 microg/ min IC) was infused along with dobutamine. Increases in CBF during dobutamine and isoproterenol were compared before and after blockade of beta1-adrenergic receptors with atenolol. Dobutamine caused proportional, dose-dependent increases in CBF, MVO2, and SS, which were not altered by L-NAME. Administration of the NO donors or ACh during dobutamine markedly decreased CPP, but only ACh also reduced SS and MVO2. These latter effects persisted after L-NAME. Atenolol blunted increases in CBF by dobutamine more than those by isoproterenol. We conclude that endogenous NO did not modulate the coronary vasodilation or the increases in myocardial contractility and MVO2 during dobutamine. In addition, neither SNP nor NTG altered myocardial contractility or MVO2 in dobutamine-stimulated myocardium, whereas ACh had a negative inotropic effect in dobutamine-stimulated myocardium that was independent of NO. ⋯ Endogenous nitric oxide (NO) did not modulate increases in coronary blood flow, myocardial contractility, or myocardial oxygen consumption during intracoronary infusions of dobutamine. The NO donors sodium nitroprusside and nitroglycerin had no effect on contractility or oxygen consumption in dobutamine-stimulated myocardium. Acetylcholine had negative inotropic effect in dobutamine-stimulated myocardium that was independent of NO.