Wright J L, Churg A
Department of Pathology, University of British Columbia, Vancouver, Canada.
Exp Lung Res. 1991 Nov-Dec;17(6):997-1009. doi: 10.3109/01902149109064331.
To investigate the effect of chronic exposure to cigarette smoke on the structure and function of the pulmonary vasculature, we used a guinea pig model of cigarette smoke-induced emphysema, in which groups of guinea pigs were exposed to smoke for periods of 1, 3, 6, and 12 months. We found that the mean pulmonary artery pressure in smokers was increased at one month, a time at which there was no evidence of emphysema. Although the vascular pressures remained elevated, they did not progressively increase, even though there was progressive lung destruction. Pulmonary hypertension was associated with muscularization of the arterioles, seen as an increase in the percentage of small pulmonary vessels with double elastic lamina. We conclude that chronic exposure to cigarette smoke will produce pulmonary hypertension in the guinea pig, and that the hemodynamic changes are accompanied by alteration of the structure of the small pulmonary arterioles and arteries. The apparent dissociation of pulmonary hypertension and emphysema suggests that the pulmonary hypertension is not due to destruction of the lung capillary bed. The etiology of this process may be smoke-induced inflammation with release of vasoactive substances as well as proteolytic enzymes.
为了研究长期接触香烟烟雾对肺血管系统结构和功能的影响，我们使用了香烟烟雾诱导的豚鼠肺气肿模型，将豚鼠分组，分别暴露于烟雾中1、3、6和12个月。我们发现，吸烟者的平均肺动脉压在1个月时升高，此时尚无肺气肿的证据。尽管血管压力持续升高，但即使存在进行性肺破坏，它们也没有逐渐增加。肺动脉高压与小动脉肌化有关，表现为具有双弹性膜的小肺血管百分比增加。我们得出结论，长期接触香烟烟雾会在豚鼠中产生肺动脉高压，并且血流动力学变化伴随着小肺小动脉和动脉结构的改变。肺动脉高压与肺气肿明显分离表明，肺动脉高压并非由于肺毛细血管床破坏所致。这一过程的病因可能是烟雾诱导的炎症，伴有血管活性物质以及蛋白水解酶的释放。
