イソフルレン麻酔の循環動態と血中カテコラミン濃度に関する実験的研究

In the present study, dogs were administered isoflurane at 3 concentrations, 1.5%, 2.2% and 3%, for 135 min. The end-tidal concentrations and blood concentrations of isoflurane were determined, and the relation between circulation dynamics and blood catecholamine concentrations was examined. In addition, the effect of a pain stimulation, given 120 min. after starting the inhalation, on the circulation dynamics and blood catecholamine concentrations was investigated. From 30 min. after the inhalation was begun, the anesthetic depth was maintained at 1MAC, 1.5MAC and 2MAC at the isoflurane inhalation concentrations of 1.5%, 2.2% and 3%, respectively. The blood isoflurane concentrations changed proportionally with the end-tidal concentrations: 9.8 mg/dl at 1MAC, 14.8 mg/dl at 1.5MAC and 19.0 mg/dl at 2MAC. The correlations between the blood isoflurane concentrations during inhalation and several parameters of circulatory dynamics were highly negative. The correlation coefficients were γ=-0.888 (mean arterial pressure), γ=-0.726 (heart rate), γ=-0.743 (cardiac index) and γ=-0.855 (left ventricular peak dp/dt/IP). On the other hand, the correlation between the blood isoflurane concentrations and the systemic vascular resistance was low (γ=-0.515). Highly negative correlations were found between the blood isoflurane concentrations during inhalation and the blood catecholamine concentrations: adrenaline, γ=-0.864; noradrenaline, γ=-0.687. The results of the present study indicate that isoflurane suppresses the circulatory dynamics, and that this suppression is due in part to the suppression of the sympathetic nervous system and adrenal system, as indicated by the blood catecholamine levels. However, while the catecholamine levels recovered after termination of the inhalation, none of the parameters of circulatory dynamics returned to pre-inhalation levels except the mean arterial pressure. The recovery of the heart rate, cardiac index and left ventricular peak dp/dt/IP was poor, indicating that myocardial suppression due to isoflurane continued even after anethesia was discontinued. The pain stimulation given 120 min into the inhalation period did not lead to any significant changes in the circulatory dynamics in any group, but it did cause a significant rise in the blood catecholamine concentration in the 1.5% (1MAC) group. This result indicates that the 1MAC isoflurane anethesia is not deep enough to block the centripetal impulse resulting from the stimulation.