Reichart E, Boerkmann P, Plenat F
Unité 14 de l'INSERM, Vandoeuvre-les-Nancy, France.
Eur Respir J. 1992 Jul;5(7):810-4.
Eight weeks after a single intravenous injection of trypsin, more than half of 26 treated rats showed pulmonary emphysema, as demonstrated by a significant increase of the mean linear intercept (MLI = 107 microns) in comparison with 11 controls (69 +/- 15 microns) (mean +/- SD). As observed 56 days after the injection, the intraperitoneal administration of trypsin (24 rats) also leads to lung emphysema (MLI = 101-106 microns), as does endotracheal instillation of elastase (13 rats), (MLI = 108 microns). The intraperitoneal administration of trypsin in animals constitutes a model close to human pathology with which lung alterations in acute pancreatitis may be studied. Having no elastolytic properties, trypsin cannot directly induce emphysema. The observation of a pulmonary leucostasis in eight rats sacrificed early after the trypsin injection suggested that leucocyte trapping and activation are important for the genesis of this trypsin-triggered emphysema.
单次静脉注射胰蛋白酶八周后，26只接受治疗的大鼠中有超过一半出现肺气肿，平均线性截距（MLI = 107微米）显著增加，相比之下，11只对照大鼠的平均线性截距为（69 +/- 15微米）（平均值 +/- 标准差）。注射后56天观察发现，腹腔注射胰蛋白酶（24只大鼠）也会导致肺气肿（MLI = 101 - 106微米），气管内注入弹性蛋白酶（13只大鼠）同样如此（MLI = 108微米）。在动物中腹腔注射胰蛋白酶构成了一个与人类病理学相近的模型，借此可以研究急性胰腺炎时的肺部改变。胰蛋白酶不具有弹性蛋白分解特性，无法直接诱发肺气肿。对注射胰蛋白酶后早期处死的8只大鼠进行观察，发现肺部白细胞淤滞，这表明白细胞滞留和激活对这种由胰蛋白酶引发的肺气肿的发生发展至关重要。
