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Korean J Anesthesiol. 2007 Jun;52(6):S25-S31. English. Original Article.
Yoo KY , Park NG , Jeong CY , Chung SS , Yoon MH , Kwak SH , Choi JI , Bae HB .
Department of Anesthesiology and Pain Medicine, Chonnam National University Medical School, Korea.
School of Dentistry, Chonnam National University Gwangju, Korea.

BACKGROUND: Endotracheal intubation often results in hypertension and tachycardia. Desflurane and nitrous oxide (N2O) are known to augment the sympathetic nervous activity. We examined whether N2O and desflurane affect the cardiovascular responses to the intubation. METHODS: One hundred-fifty patients were assigned randomly to receive one of six treatment regimens (n = 25 each): 2% sevoflurane (control), 6% desflurane or 12% desflurane with and without 75% N2O, respectively. General anesthesia was induced with intravenous thiopental (5-7 mg/kg), and tracheal intubation was facilitated with intravenous vecuronium (0.12 mg/kg). N2O was started 3 min before and desflurane soon after the intubation. Systolic arterial blood pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were determined. RESULTS: The intubation increased SAP and HR in all groups within 1 min. A second increase was noted with 12% desflurane at 3 to 5 min after the intubation. N2O did not affect the tachycardiac response, but attenuated the pressor response to both intubation and 12% desflurane. The plasma concentrations of norepinephrine increased significantly at 1 min after the intubation in all groups with more pronounced rise in N2O groups, and increased further at 5 min in the 12% desflurane groups. CONCLUSIONS: A biphasic increase of SAP and HR was noted with 12% desflurane. The first increase may be related with the mechanical stimulus of the tracheal intubation and the second with the desflurane itself. Although N2O did not affect the tachycardiac responses and augmented norepinephrine release, it suppressed the pressor responses.

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