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[实验性创伤性休克中的胰蛋白酶-抗胰蛋白酶系统及血液中分子肽含量]

[The trypsin-antitrypsin system and the content of blood middle-molecular peptides in experimental traumatic shock].

作者信息

Gudumak V S, Marchenko V P, Nigulianu V I

出版信息

Patol Fiziol Eksp Ter. 1990 Mar-Apr(2):30-2.

PMID:1696370
Abstract

It was established that the activity of trypsin and the content of its inhibitors--alpha 1-inhibitor of proteinases and alpha 2-macroglobulin--undergo phase changes of different meaning and direction with the gradual development of traumatic shock. The character of these changes indicates that trypsinemia is an important pathogenetic link of traumatic shock and corresponds to its severity. The compensatory activation of the trypsin inhibitors is directed to increasing the resistance of the body to trypsinemia. Deficiency of the inhibition system leads to activation of organic proteolysis and growth of the content of middle-molecular peptides in the blood. Such a character of homeostasis disorders substantiates the need for the search for effective measures of correction of the trypsin-antitrypsin system and freeing the organism of the excess of middle-molecular molecules.

摘要

已确定随着创伤性休克的逐渐发展,胰蛋白酶的活性及其抑制剂——蛋白酶α1抑制剂和α2巨球蛋白的含量会发生不同意义和方向的阶段性变化。这些变化的特征表明,胰蛋白酶血症是创伤性休克的一个重要发病机制环节,且与休克的严重程度相对应。胰蛋白酶抑制剂的代偿性激活旨在增强机体对胰蛋白酶血症的抵抗力。抑制系统的缺陷会导致有机蛋白水解的激活以及血液中中分子肽含量的增加。内稳态紊乱的这种特征证实了寻找纠正胰蛋白酶 - 抗胰蛋白酶系统的有效措施以及清除机体中过量中分子物质的必要性。

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