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以肺泡缺氧5 min时肺阻抗血流图波幅降低的百分率(△H％)作为肺血管收缩反应强度的指标。实验结果表明:吸烟使人缺氧性肺血管收缩反应增强,吸烟前后的△H％分别为17.62±2.92％和29.68±4.28％(P<0.01);用乙胺嗪后吸烟增强肺血管反应性的作用明显减弱,这提示白三烯在吸烟引起肺血管对缺氧反应性增强中起介导作用。
The percentage of decrease of amplitude of pulmonary impedance blood flow (△ H%) at 5 min after alveolar anoxia was used as an index of the intensity of pulmonary vasoconstriction. The experimental results showed that the hypoxic pulmonary vasoconstriction was enhanced by smoking, and the △ H% before and after smoking were 17.62 ± 2.92% and 29.68 ± 4.28%, respectively (P <0.01). Smoking with diethylcarbamazine increased the pulmonary vascular reactivity The role of significantly weakened, suggesting that leukotriene in smoking caused pulmonary vascular hypoxia reactivity enhancement played a mediating role.