Abstract

Background: Endotracheal intubation in patients undergoing general anesthesia often causes hypertension and tachycardia. Nitrous oxide (), which is frequently used during the induction of anesthesia, is known to augment sympathetic nervous activity in humans. The aim of the present study was to investigate whetheraffects cardiovascular response to intubation. Methods: After IRB approval, 100 ASA I patients (aged 35-60 yr) were assigned randomly to receive one of four concentrations (0, 25, 50 or 75%;n = 25 for each) ofin oxygen throughout the study period, beginning 3 min before intubation. Anesthesia was induced with IV thiopental (5-7 mg/kg) and tracheal intubation was faciliated with IV vecuronium (0.12 mg/kg), while patients were ventilated with the designated concentrations ofin oxygen. After intubation, all patients received 2% sevoflurane andin oxygen via a semiclosed anesthesia circuit. Systolic arterial pressure (SAP), heart rate (HR) and rhythm were recorded before and after intubation at intervals for up to 5 min. Plasma concentrations of catecholamines were measured before and 3 min after induction, and 1 and 5 min after intubation. Results: The intubation caused significant increases in SAP and HR in all groups (P < 0.05). Increasing concentrations ofgradually attenuated the pressor response to intubation, without affecting the tachycardiac response. No significant differences were observed between the groups in plasma concentrations of either norepinephrine or epinephrine: norepinephrine concentration increased significantly 1 min after intubation in all -treated groups, while it remained unchanged in the control group. In contrast, the epinephrine concentration remained unaltered in all -treated groups, but increased significantly in the control group. Incidence of tachycardia, bradycardia, and arrhythmia was not different among the groups. Conclusions: These results indicate thatsuppresses the pressor but not the tachycardiac response associated with endotracheal intubation, while it enhances the increases in plasma norepinephrine concentrations.

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