Kobayashi H, Hobara T, Kawamoto T, Sakai T
Arch Environ Health. 1987 May-Jun;42(3):140-3. doi: 10.1080/00039896.1987.9935811.
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.
在急性吸入实验中，对麻醉犬吸入急性1,1,1-三氯乙烷（1,1,1-TCE）时心率的反应及其通过自主神经系统的机制进行了研究。吸入气中1,1,1-TCE浓度为1.32±0.14%（平均值±标准误）时心率增加，但浓度为2.79±0.24%时心率降低。吸入后血压降至70-80 mmHg时观察到心率的相反反应。此外，预先给予肾上腺素β受体阻滞剂可阻断相对低浓度引起的心动过速和高浓度引起的心动过缓，但迷走神经切断术对其影响较小。提示吸入1,1,1-TCE后的心动过速和心动过缓可能均由交感神经系统控制。
