Effect of ozone on bronchomotor response to inhaled histamine aerosol in dogs.
Effect of ozone on bronchomotor response to inhaled histamine aerosol in dogs.
复制标题
臭氧对狗吸入组胺气溶胶支气管运动反应的影响。
DOI：
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发表时间：
1977
期刊：
影响因子：
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通讯作者：
J. Nadel
中科院分区：
文献类型：
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作者：
L. Lee;E. Bleecker;J. Nadel
为研究臭氧对二磷酸组胺气雾剂吸入支气管反应性的影响，我们在5只狗上进行了14个实验，狗用戊巴比妥钠（25-30 mg/kg，iv）麻醉，用哈佛呼吸器通气。在臭氧暴露之前，吸入组胺气雾剂（2%溶液; 5次呼吸）使总肺阻力（RL）增加5.1 +/- 0.5 cmH 2 O/1/s（平均值+/- SE）。臭氧暴露后1天（0.7-1.2 ppm; 2 h），基线RL无显著变化（P> 0.05），但组胺引起的RL增加（10.7 +/- 1.1 cmH 2 O/1/s）大于对照状态（P <0.01）。当狗用硫酸阿托品气雾剂（1.5%溶液; 10次呼吸）预处理时，组胺后RL的增加降低至臭氧前的3.8 +/- 0.3 cmH 2 O/1/s，臭氧后无显著差异（4.5 +/- 1.1 cmH 2 O/1/s; P> 0.5）。迷走神经传导的冷却阻滞可减少组胺后RL的增加，臭氧前为每秒3.9 +/- 0.5 cmH 2 O/1，臭氧后无显著差异（每秒4.4 +/- 0.6 cmH 2 O/1; P小于0.5）。由于阿托品和迷走神经冷却取消臭氧引起的支气管过敏，我们得出结论，它是通过迷走神经胆碱能通路介导的。
To study the effect of ozone on bronchial reactivity to inhaled histamine diphosphate aerosol, we performed 14 experiments on 5 dogs anesthetized with pentobarbital sodium (25-30 mg/kg, iv) and ventilated with a Harvard respirator. Prior to ozone exposure, inhalation of histamine aerosol (2% solution; 5 breaths) increased total pulmonary resistance (RL) 5.1 +/- 0.5 cmH2O/1 per s (mean +/- SE). One day after ozone exposure (0.7-1.2 ppm; 2 h), the base-line RL was not significantly changed (P greater than 0.05), but the increase of RL caused by histamine (10.7 +/- 1.1 cmH2O/1 per s) was greater than in the control state (P less than 0.01). When the dogs were pretreated with atropine sulfate aerosol (1.5% solution; 10 breaths), the increase of RL after histamine was decreased to 3.8 +/- 0.3 cmH2O/1 per s before ozone, and this was not significantly different after ozone (4.5 +/- 1.1 cmH2O/1 per s; P greater than 0.5). Cooling blockade of conduction in the vagus nerves diminished the increase of RL after histamine to 3.9 +/- 0.5 cmH2O/1 per s before ozone, and this was not significantly different after ozone (4.4 +/- 0.6 cmH2O/1 per s; P less than 0.5). Since both atropine and vagal cooling abolished the ozone-induced bronchial hyperirritability, we conclude that it is mediated via vagal cholinergic pathways.