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实验性内源性革兰氏阴性菌腹膜炎中的血管活性肠肽和生长抑素

Vasoactive intestinal polypeptide and somatostatin in experimental endogenous gram-negative peritonitis.

作者信息

Almdahl S M, Jenssen T G, Burhol P G, Giercksky K E

出版信息

Acta Chir Scand. 1986 Feb;152:135-8.

PMID:2869631
Abstract

Vasoactive intestinal polypeptide (VIP) and somatostatin were measured during endogenous gram-negative peritonitis and septicaemia in rats. Both peptides were found to increase in blood, but not in peritoneal fluid. The VIP values coincided with the levels of endotoxin and bacterial counts. However, if the development of profound shock was prevented by intravenous fluid supply, scarcely any changes in plasma VIP or somatostatin were found. Somatostatin is known to inhibit VIP. Our findings suggested breakdown of this regulatory inhibition in lethal gram-negative sepsis. They also supported the concept that specific release of the peptides takes place, not merely passive diffusion from injured cells.

摘要

在大鼠内源性革兰氏阴性菌腹膜炎和败血症期间,检测了血管活性肠肽(VIP)和生长抑素。发现这两种肽在血液中增加,但在腹腔液中未增加。VIP值与内毒素水平和细菌计数一致。然而,如果通过静脉补液防止严重休克的发生,则血浆VIP或生长抑素几乎没有变化。已知生长抑素会抑制VIP。我们的研究结果表明,在致命的革兰氏阴性菌败血症中,这种调节性抑制作用被破坏。它们还支持这样一种观点,即这些肽是特异性释放的,而不仅仅是从受损细胞被动扩散而来。

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