Wright J L, Churg A
Department of Pathology, University of British Columbia, Vancouver, Canada.
Am J Physiol. 1995 Jan;268(1 Pt 1):L17-20. doi: 10.1152/ajplung.1995.268.1.L17.
We have previously shown that chronic cigarette smoke exposure produces emphysema and airflow obstruction in the guinea pig. To further examine the changes in the connective tissue matrix associated with emphysema in this model, we used ultrastructural morphometry to determine the volume proportions of collagen and elastin in the alveolar walls of animals exposed to smoke or air (control) for 1, 3, 6, and 12 mo. After 1 mo of smoke exposure, there was a statistically significant (P < 0.001) decrease in the volume proportion of collagen in the smoke-exposed animals, whereas by 6 and 12 mo of smoke exposure, the proportion of collagen had significantly (P < 0.02, P < 0.03, respectively) increased. The volume proportion of elastin was increased in the smoke-exposed animals at the 12-mo time period. While our results do not exclude reorganization of elastin within the alveolar wall, we conclude that, in this model, cigarette smoke-induced emphysema appears to be associated with collagen breakdown and repair. We suggest that the currently accepted proteolysis-antiproteolysis theory is too narrow in its focus on elastin destruction as the major contributor to emphysema and should be broadened to the concept that smoke-induced emphysema reflects breakdown and resynthesis (possibly overproduction in the form of scarring) of a variety of connective tissue proteins in addition to elastin.
我们之前已经表明，长期暴露于香烟烟雾会在豚鼠身上导致肺气肿和气流阻塞。为了进一步研究该模型中与肺气肿相关的结缔组织基质的变化，我们使用超微结构形态计量学来确定暴露于烟雾或空气（对照）1、3、6和12个月的动物肺泡壁中胶原蛋白和弹性蛋白的体积比例。暴露于烟雾1个月后，暴露于烟雾的动物中胶原蛋白的体积比例出现统计学显著下降（P < 0.001），而到暴露于烟雾6个月和12个月时，胶原蛋白的比例显著增加（分别为P < 0.02，P < 0.03）。在12个月时，暴露于烟雾的动物中弹性蛋白的体积比例增加。虽然我们的结果不排除弹性蛋白在肺泡壁内的重新组织，但我们得出结论，在这个模型中，香烟烟雾诱导的肺气肿似乎与胶原蛋白的分解和修复有关。我们认为，目前被接受的蛋白水解 - 抗蛋白水解理论过于狭隘地将弹性蛋白破坏视为肺气肿的主要促成因素，应该扩展到这样一个概念，即烟雾诱导的肺气肿反映了除弹性蛋白之外的多种结缔组织蛋白的分解和重新合成（可能以瘢痕形成的形式过度产生）。
