The effect of remifentanil infusion on coughing during emergence from general anesthesia with desflurane / 대한마취과학회지

BACKGROUND: Coughing during emergence from general anesthesia is a common clinical problem and results in a number of undesirable side effects. Remifentanil stimulate micron-opioid peptide receptor known to be related to antitussive effect. The goal of this study was to evaluate the effect of remifentanil on coughing after general anesthesia with desflurane. METHODS: Fifty one ASA physical status I and II patients undergoing elective oral and maxillofacial surgery were randomly assigned to receive either remifentanil with 1 ng/ml effect site concentration or normal saline until extubation. The number and intensity of coughs were monitored during emergence and the recovery time was recorded. RESULTS: The incidence and number of coughing during emergence was significant less frequent in the remifentanil group (P < 0.05). The intensity of coughing was significant milder in the remifentanil group (P < 0.05). There was no significant difference between two groups in the recovery time. CONCLUSIONS: Continuous remifentanil infusion with 1 ng/ml effect site concentration during emergence from general anesthesia with desflurane decrease the incidence of coughing without delaying the recovery time.

Effects of Propofol on Arginine Vasopressin-induced Contraction in Isolated Human Gastroepiploic Artery / 대한마취과학회지

BACKGROUND: Arginine vasopressin has been used by prophylactic treatment of vasodilatory shock during coronary artery bypass graft (CABG). Vasopressin may be a cause of spasm in graft artery during CABG. We evaluated the effect of propofol on vasopressin-induced contraction in human gastroepiploic artery (GEA). METHODS: Human GEA were obtained from 35 patients (43-74 yr), undergoing subtotal gastrectomy. Vasopressin-induced a concentration contractions (10(-9) to 10(-6) M) were measured after exposed to without propofol, propofol 10(-5), 10(-4), 10(-3) M. After endothelium denuding vasopressin-induced a concentration contractions were measured with or without propofol 10(-3) M in calcium free solution. In the denuded vascular rings, with or without pretreatment of glibenclamide (10(-5) M), nicorandil (10(-5) M), or diltiazem (10(-5) M) were exposed to with or without propofol 10(-3) M, and vasopressin-induced concentration contractions were measured. RESULTS: Vasopressin-induced concentration contraction on human GEA was independent of functional endothelium. Propofol (10(-4), 10(-3) M) attenuated the vasopressin-induced contraction in the human GEA. Diltiazem attenuated the vasopressin-induced contraction in the human GEA. ATP-sensitive potassium channel does not affect the inhibition effect of propofol on vasopressin-induced contraction CONCLUSIONS: Usual anesthetic dose of propofol does not inhibit vasopressin-induced contraction on human GEA. High dose (>10(-4) M) propofol attenuated vasopresssi-induced contraction on GEA.