Martorana P A, Share N N
Am Rev Respir Dis. 1976 May;113(5):607-12. doi: 10.1164/arrd.1976.113.5.607.
The possibility that human alpha1-antitrypsin could effectively prevent development of emphysematous lesions produced in hamsters 7 days after exposure to aerosolized papain (3% for 3 hours) was investigated. Pretreatment with intratracheal human alpha1-antitrypsin prevented the appearance of these lesions in a dose-dependent manner. On the other hand, systemic administration of large doses of human alpha1-antitrypsin failed to prevent papain-induced pulmonary lesions, despite a significant increase in serum trypsin inhibitory capacity. These results suggest that intra-alveolar rather than serum concentrations of human alpha1-antitrypsin are critical for preventing the development of pulmonary emphysema in this animal model. It is interesting that although the mechanism by which human alpha1-antitrypsin prevented the papain-induced lesions is unknown, intratracheally administered human alpha1-antitrypsin similarly prevented the development of pulmonary emphysematous lesions induced by 0.1 mg of porcine pancreatic elastase given intratracheally.
研究了人α1-抗胰蛋白酶能否有效预防仓鼠在雾化吸入木瓜蛋白酶(3%,3小时)7天后产生的肺气肿病变。气管内给予人α1-抗胰蛋白酶预处理可呈剂量依赖性地预防这些病变的出现。另一方面,尽管血清胰蛋白酶抑制能力显著增加,但全身给予大剂量人α1-抗胰蛋白酶未能预防木瓜蛋白酶诱导的肺部病变。这些结果表明,在该动物模型中,肺泡内而非血清中的人α1-抗胰蛋白酶浓度对于预防肺气肿的发展至关重要。有趣的是,尽管人α1-抗胰蛋白酶预防木瓜蛋白酶诱导病变的机制尚不清楚,但气管内给予人α1-抗胰蛋白酶同样能预防气管内给予0.1 mg猪胰弹性蛋白酶诱导的肺气肿病变的发展。