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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.