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本文研究吸烟引起的缺氧性肺血管收缩反应(HPV)的变化与动物种属及吸烟时间的关系,以及肺血管反应性变化的机制。以肺血管阻力变化百分率(△PVR%)或肺阻抗血流图收缩波波幅变化率(△H%)作为缺氧性肺血管收缩反应强度的指标。实验结果发现,急性吸烟使大鼠的HPV增强(△PVR%从55.0±15.6%增至102.3±12.4%),主要由白三烯介导;使幼猪的HPV减弱(△PVR%从65.2±12.5%减至55.9±9.8%),主要由肾上腺素β受体介导;使人的HPV增强(△H%从20.6±2.6%增至31.1±4.1%),前列腺素和白三烯起介导作用。大鼠吸烟一个月后HPV反而下降(△PVR%为11.4±6%,同期对照组为31.1±0.8%),与扩管性前列腺素增多和白三烯生成减少有关。
This article studies the relationship between smoking-induced hypoxic pulmonary vasoconstriction (HPV) changes and animal species and smoking time, and the mechanism of pulmonary vascular reactivity changes. The percent change of pulmonary vascular resistance (△ PVR%) or the rate of change of pulmonary wave impedance (△ H%) was used as an indicator of hypoxic pulmonary vasoconstriction. The results showed that acute smoking increased the HPV level (△ PVR% from 55.0 ± 15.6% to 102.3 ± 12.4%) and was mainly mediated by leukotrienes. The piglets had weakened HPV (△ PVR% from 65.2 ± 12.5% to 55.9 ± 9.8%), mainly by the adrenergic β receptor; increased HPV in humans (△ H% from 20.6 ± 2.6% to 31.1 ± 4.1%), prostaglandins and leukotrienes Guide role. In one month after smoking, HPV decreased (ΔRVR% 11.4 ± 6% in the control group during the same period was 31.1 ± 0.8%), increased with expanded prostaglandin and decreased leukotriene production.