[Lymph drainage disorder as a pathogenetic co-factor in acute pancreatitis?].

H P Putzke, M Müller, E Siegmund, W Dummler
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Abstract

Experiments performed on 71 Wistar rats confirm that preexisting interruption of lymph drainage by ligation of the ductus thoracicus can have a major influence on the development of pancreatitis. The effect of a ductus hepatopancreaticus blockade in experimental group A (32 animals) was greatly exacerbated by previous ligation of the ductus thoracicus (experimental group B; 34 animals). Edema of the interstitial pancreatic tissue led to lipolytic necrotizing pancreatitis with a slight hemorrhagic component, increasing ascites after the 12 th hour of the experiment, and numerous abdominal fat necroses after about 19 hours, but only relatively minor necroses of acinar parenchyma cells in the pancreas. Fat tissue necroses were only found in almost 20% of the animals in group A, and these probably resulted from manipulation of the duodenum during the implantation of a shunt to divert the bile, whereas they were found in all animals of group B after the 19th hour of the experiment, usually in large numbers. The sometimes considerable increases in serum amylase and particularly lipase activity were caused by obstruction of the efferent ducts, but did not increase appreciably after disturbance of the lymph drainage systems. On the contrary, under these circumstances, drainage of the salivary edema via the peritoneal mesothelium and into retroperitoneal fat tissue must be considered responsible for ascites and the initiation of fat cell necroses by lipase and other enzymes.

[淋巴引流障碍是急性胰腺炎的致病因子?]。
在71只Wistar大鼠身上进行的实验证实,先前存在的胸导管结扎导致的淋巴引流中断可能对胰腺炎的发展有重要影响。实验a组(32只)经胸胰管结扎后肝胰管阻滞的效果明显加重(实验B组;34动物)。胰腺间质组织水肿导致溶脂性坏死性胰腺炎,伴有轻微出血性成分,实验第12小时后腹水增多,约19小时后腹部大量脂肪坏死,但胰腺腺泡实质细胞只有相对较小的坏死。A组只有近20%的动物出现脂肪组织坏死,这可能是由于在植入分流器时对十二指肠的操作导致的,而B组在实验第19小时后所有动物都出现了脂肪组织坏死,通常是大量的。有时血清淀粉酶,特别是脂肪酶活性的显著增加是由传出管阻塞引起的,但在淋巴排水系统紊乱后没有明显增加。相反,在这种情况下,唾液水肿通过腹膜间皮引流到腹膜后脂肪组织,必须被认为是腹水和脂肪酶和其他酶引发脂肪细胞坏死的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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