1,1,1-Trichloroethane吸入による降圧機序

抄録

It is reported that circulatory shock following inhalation of 1, 1, 1-trichloroethane (1, 1, 1-TCE) at high concentrations may be related to the cause of death. However, a mechanism of the fall in the blood pressure due to 1, 1, 1-TCE inhalation is still uncertain. The purpose of this experiment was to investigate the mechanism of systemic hypotension due to 1, 1, 1-TCE inhalation using hemodynamic and neuroelectrophysiologic technics. Adult fifty mongrel dogs were anesthetized with sodium pentobarbital, injected at 25-30 mg/kg intravenously. Tracheal intubation was performed, and experiment was carried out under positive pressure ventilation. Various concentrations of 1, 1, 1-TCE vapor were made by an inside circuit vaporizer to be inhaled during a period of thirty seconds to two minutes. Concentrations of 1, 1, 1-TCE in the inspired air were measured by gas chromatography. Aortic blood flow and pressure were measured by an electromagnetic flow meter (Nihon Kohden, MFV-1100) and a strain gauge transducer (Nihon Kohden, MPU-0.5), respectively, in thoracotomized dogs. Total peripheral vascular resistance (T.P.R.) was calculated from aortic blood pressure/aortic blood flow. After incision of the left flank, left kidney was exposed. Then the efferent renal sympathetic nerve activity was recorded using bipolar platinum electrodes. In acute inhalation experiment, the threshold concentration of 1, 1, 1-TCE to produce a fall in blood pressure was 0.4 to 0.5% in inspired air, and a dose-response relationship between the fall in the blood pressure and the concentration of 1, 1, 1-TCE which exceeded the threshold level was observed. T.P.R. obviously decreased during inhalation, and gradually returned to pre-inhalation level after termination of inhalation. Therefore, it is suggested that the fall in the blood pressure following 1, 1, 1-TCE inhalation may be related to the decrease in T.P.R. In addition, a doseresponse relationship between the change of T.P.R. and the concentration of 1, 1, 1-TCE was observed. Efferent renal sympathetic nerve activity increased, associated with a slight fall in the blood pressure, following inhalation of relative low concentrations of 1, 1, 1-TCE, whereas, renal sympathetic nerve activity decreased, accompanied with a marked decrease in the blood pressure, following inhalation of high 1, 1, 1-TCE concentrations. Such reversion as the effect of the renal sympathetic nerve activity was observed in the range of the lowered blood pressure level at 70-80 mmHg, following inhalation of intermediate concentration of 1, 1, 1-TCE. Reactions of the renal sympathetic nerve activity following inhalation were not affected by bilateral cervical vagotomy. On the other hand, the increase in the renal sympathetic nerve activity following inhalation of relatively low concentrations was disappeared by transection of both vagi and carotid sinus nerves. However, the decrease in the activity following inhalation of high concentrations was not affected by such transection. From these results, it is suggested that systemic hypotension due to 1, 1, 1-TCE inhalation at high concentrations may be related to the decrease in T.P.R., and may be induced by a mechanism which is not related to the sympathetic nervous system and other neurogenic mechanisms.