Willemer S, Feddersen C O, Karges W, Adler G
Department of Internal Medicine, Philipps-University Marburg, FRG.
Int J Pancreatol. 1991 May;8(4):305-21. doi: 10.1007/BF02952723.
The pathogenesis of pancreatitis-related pulmonary injury was studied at the light- and electronmicroscopic level. Experimental pancreatitis was induced in rats by infusion of supramaximal doses of cerulein for 12 h. Investigations were carried out 3, 6, and 12 h after the start of infusion and 12, 48, and 72 h after the end of pancreatitis induction. Initial manifestations of pancreatitis-associated lung injury revealed a pronounced clustering of polymorphonuclear leukocytes in pulmonary microvessels, followed by severe damage of alveolar endothelial cells. Consecutively, the increase in vascular permeability of the lung resulted in interstitial edema formation. Structural changes were maximal after 12 h and reversed completely after 84 h. In conclusion, the structural appearance of pulmonary injury in cerulein-induced pancreatitis was similar to that reported in early stages of the adult respiratory distress syndrome (ARDS). It is suggested that polymorphonuclear granulocytes play a crucial role in the pathogenesis of pancreatitis-related lung injury.
在光学显微镜和电子显微镜水平上研究了胰腺炎相关性肺损伤的发病机制。通过输注超最大剂量的雨蛙肽12小时,在大鼠中诱导实验性胰腺炎。在输注开始后3、6和12小时以及胰腺炎诱导结束后12、48和72小时进行研究。胰腺炎相关性肺损伤的初始表现为肺微血管中多形核白细胞明显聚集,随后肺泡内皮细胞严重受损。接着,肺血管通透性增加导致间质水肿形成。结构变化在12小时后最大,并在84小时后完全逆转。总之,雨蛙肽诱导的胰腺炎中肺损伤的结构表现与成人呼吸窘迫综合征(ARDS)早期报道的相似。提示多形核粒细胞在胰腺炎相关性肺损伤的发病机制中起关键作用。