| Abstract | 「Abstract」It is known that a rapid increase in isoflurane concentration elicits transient circulatory stimulation associated with plasma catecholamine elevations. Since clonidine, a relative selective α2-agonist, inhibits release of catecholamine from the sympathetic nerve endings, the authors examined whether clonidine as an oral preanesthetic medication would suppress these hemodynamic and catecholamine responses. Twenty-five patients (aged 18-55yr) randomly received either oral clonidine approximately 5 μg/kg (n=12) or no clonidine (n=13). Following anesthesia induction and tracheal intubation with thiamylal 5 mg/kg and vecuronium 0.2 mg/kg iv, anesthesia was maintained with an end-tidal concentration of isoflurane (ETISO) of 1.3%, and a fresh gas flow of air 10 L/min plus oxygen 2 L/min via a semi-closed circuit system. A radial arterial catheter was placed for monitoring of arterial pressure (AP) and for blood sampling for plasma norepinephrine (NE) and epinephrine (E) assay. After stable anesthesia with ETISO of 1.3 % for 15 min, the ETISO was maintained at 2.6 % for 10 min by increasing the inspired concentration and adjusting the vaporizer setting. After increasing the concentration of isoflurane, AP and heart rate (HR) values were recorded every minute for 10 min, while plasma NE and E levels were measured at baseline and at 1, 2, 3, 5, and 10 min. Data collection was completed in 10 and 12 patients, since systolic AP decreased below 70 mmHg in 2 and 1 patients of the clonidine and control groups, respectively, within 1-4 min following abrupt increase in ETISO (P>0.05 in the incidence of hypotension between groups). Systolic and diastolic APs were lower in the clonidine group than the control group before abrupt ETISO elevation (P<0.05). Following rapid increase in isoflurane concentration, significant elevations from baseline values (P<0.05) were noted in systolic AP at 2-min recording (18±3 mmHg, mean±SE) and in diastolic AP at 1-min (12±3 mmHg) and 2-min recordings (16±3 mmHg) in the control group. However, the clonidine group did not show significant transient AP increases, and a significant difference between groups (P<0.05) was found only in diastolic AP changes from baselines at 1 min after the high isoflurane challenge. Although HR increased from baseline values in both groups for approximately 6 min after the high isoflurane challenge, the magnitudes of HR increases were similar between groups. Plasma NE levels and E levels were less in the clonidine group than the control group throughout the study, while plasma E levels were less in the clonidine group before and at 5 and 10 min after the high isoflurane exposure (P<0.05). However, they increased in all patients of both groups following abrupt increase in ETISO. In addition, no intergroup difference was observed in the magnitudes of increases in plasma NE and E levels. These results suggest that oral preanesthetic medication of clonidine 5 μg/kg medication partially attenuates the pressor response but does not suppress the heart rate and catecholamine responses to a rapid increase in isoflurane concentration. |
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