Effect of 1,1,1-Trichloroethane Inhalation on Heart Rate and Its Mechanism: A Role of Autonomic Nervous System

Abstract
The response of heart rate to acute 1,1,1-trichloroethane (1,1,1-TCE) inhalation and its mechanism via the autonomic nervous system were studied in anesthetized dogs in acute inhalation experiments. Concentrations of 1,1,1-TCE in inspired air of 1.32 .+-. 0.14% (mean .+-. S.E.) increased heart rate, but 2.79 .+-. 0.24% decreased heart rate. Opposite reactions of heart rate were observed when blood pressure decreased to 70-80 mm Hg following inhalation. Moreover, both tachycardia from relatively low concentrations and bradycardia from higher concentrations were blocked by pre-administration of adrenergic beta blocker, but were only slightly affected by vagotomy. It is suggested that both tachycardia and bradycardia following 1,1,1-TCE inhalation may be controlled by the sympathetic nervous system.