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[淋巴引流障碍作为急性胰腺炎发病机制中的一个共同致病因素?]

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

作者信息

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

机构信息

Institut für Pathologische Anatomie der Universität Rostock, DDR.

出版信息

Gastroenterol J. 1990;50(3):149-52.

PMID:2288656
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.

摘要

对71只Wistar大鼠进行的实验证实,预先通过结扎胸导管中断淋巴引流可对胰腺炎的发展产生重大影响。在实验组A(32只动物)中,肝胰管阻塞的影响在先前结扎胸导管后(实验组B;34只动物)大大加剧。胰腺间质组织水肿导致脂解性坏死性胰腺炎,伴有轻微出血成分,实验第12小时后腹水增加,约19小时后出现大量腹部脂肪坏死,但胰腺腺泡实质细胞仅有相对轻微的坏死。脂肪组织坏死仅在实验组A中约20%的动物中发现,这些可能是由于在植入分流管以引流胆汁时对十二指肠的操作所致,而在实验第19小时后,实验组B的所有动物中均发现脂肪组织坏死,且通常数量较多。血清淀粉酶尤其是脂肪酶活性有时会显著升高,这是由传出导管阻塞引起的,但在淋巴引流系统受到干扰后并未明显升高。相反,在这种情况下,唾液性水肿通过腹膜间皮引流到腹膜后脂肪组织中,必须被认为是腹水以及脂肪酶和其他酶引发脂肪细胞坏死的原因。

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