Effect of 1,1,1-trichloroethane inhalation on heart rate and its mechanism: a role of autonomic nervous system.
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.
D000280:Administration, Inhalation; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001919:Bradycardia / Q000139:chemically induced; D004285:Dogs; D005260:Female; D006339:Heart Rate / Q000187:drug effects*; D006843:Hydrocarbons, Chlorinated / Q000633:toxicity*; D008297:Male; D011433:Propranolol / Q000494:pharmacology; D013610:Tachycardia / Q000139:chemically induced; D014240:Trichloroethanes / Q000633:toxicity*; D014628:Vagotomy
D006843:Hydrocarbons, Chlorinated; D014240:Trichloroethanes; C024566:1,1,1-trichloroethane; D011433:Propranolol