Lasson A, Jönsson K, Lore'n I, Sternby N H
Department of Surgery, Malmö General Hospital, University of Lund, Sweden.
Int J Pancreatol. 1994 Aug;16(1):23-9. doi: 10.1007/BF02925606.
The possible in vivo consequences of proteolytic activity found in pancreatic pseudocyst fluid was investigated experimentally using fresh vessels from rabbit and humans. Proteolytic pseudocyst fluid caused a pronounced and time-dependent decrease in breaking strength of fresh vessels. A destruction of the normal histological architecture and fragmentation of the elastic tissue of the vessel wall paralleled the mechanical findings. The proteolytic digestion was caused by the low-mol-wt fraction of the pseudocyst fluid, corresponding to free proteases. Part of this proteolysis was probably caused by pancreatic proteases, since pancreatic juice also caused a decrease in breaking strength and a destruction of the histologic architecture of the vessel wall. Proteases bound to protease inhibitors, i.e., to alpha-2-macroglobulin, had no proteolytic activity. It is concluded that the proteolytic digestion caused by proteolytic pancreatic pseudocyst fluid may well explain severe complications of pancreatic pseudocysts, like bleeding within the pseudocyst and rupture of the entire pseudocyst wall, although the proteolytic digestion is probably counteracted by a constant regeneration of the pseudocyst wall in vivo.
利用来自兔子和人类的新鲜血管,通过实验研究了胰腺假性囊肿液中蛋白水解活性可能产生的体内后果。蛋白水解性假性囊肿液导致新鲜血管的断裂强度显著且随时间下降。血管壁正常组织学结构的破坏以及弹性组织的碎片化与力学结果相平行。蛋白水解消化是由假性囊肿液的低分子量部分引起的,这部分对应于游离蛋白酶。这种蛋白水解作用部分可能是由胰腺蛋白酶引起的,因为胰液也会导致血管壁断裂强度下降和组织学结构破坏。与蛋白酶抑制剂(即α-2-巨球蛋白)结合的蛋白酶没有蛋白水解活性。得出的结论是,蛋白水解性胰腺假性囊肿液引起的蛋白水解消化很可能解释了胰腺假性囊肿的严重并发症,如假性囊肿内出血和整个假性囊肿壁破裂,尽管在体内假性囊肿壁的持续再生可能会抵消蛋白水解消化作用。