Payen D, Bernard C, Beloucif S
Department of Anesthesiology and Critical Care Medicine, Lariboisière University Hospital, Paris, France.
Clin Chest Med. 1996 Jun;17(2):333-50. doi: 10.1016/s0272-5231(05)70318-x.
The synthesis of nitric oxide (NO) and its targets are reviewed physiologically during sepsis and wound healing, a self-limiting process in which mechanisms are still identified incompletely. NO also plays an active and direct role during infection, aimed at protecting the host and destroying the microbe. During septic shock, an overproduction of NO has been described experimentally and clinically that might be responsible for the systemic vasodilatation with hyporesponsiveness to exogenous vasoconstrictive agents. The different manipulations of NO pathway during sepsis are described (transcription and post-transcription of iNOS, enzymatic function, substrate availability, NO concentration, and NO effector molecules), although their clinical benefit remains controversial.
本文综述了脓毒症和伤口愈合(一个自我限制过程,其机制仍未完全明确)期间一氧化氮(NO)的合成及其作用靶点。NO在感染过程中也发挥着积极且直接的作用,旨在保护宿主并消灭微生物。在脓毒性休克期间,实验和临床研究均表明NO产生过多,这可能是导致全身血管扩张以及对外源性血管收缩剂反应性降低的原因。文中描述了脓毒症期间对NO途径的不同调控方式(诱导型一氧化氮合酶的转录和转录后调控、酶功能、底物可用性、NO浓度以及NO效应分子),尽管其临床益处仍存在争议。