Lorente J A, Delgado M A, Landín L
Unidad de Cuidados Intensivos, Hospital Universitario de Getafe, Madrid.
Enferm Infecc Microbiol Clin. 1997 Oct;15 Suppl 3:14-9.
Refractory hypotension is the main cause of death of patients with septic shock. It has been shown that an excessive release of NO is responsible for the sepsis-induced hypotension and vascular hyporeactivity. Nitric oxide is produced under normal conditions by a constitutive enzyme present, among other cell types, in the endothelial cell, and is necessary for maintenance of normal organ perfusion. Under inflammatory or septic conditions, a new enzyme is expressed in phagocytic cells and vascular smooth muscle cells, giving rise to an uncontrolled NO production that is associated with cytotoxic effects and vasodilatation. Randomized clinical trials have shown that the administration of inhibitors of NO synthesis to patients with septic shock is associated with a greater incidence of shock resolution, without significant adverse effects. The recent discovery of the different biological functions of NO, both under normal and inflammatory conditions, has allowed the development of new concepts about the pathophysiology of septic shock, and has provided the bases to design novel therapeutic strategies for the treatment of septic shock, based on the inhibition of NO synthesis.
难治性低血压是脓毒症休克患者死亡的主要原因。研究表明，一氧化氮（NO）的过度释放是脓毒症诱导的低血压和血管反应性降低的原因。在正常情况下，内皮细胞等多种细胞类型中存在的一种组成型酶可产生一氧化氮，它对于维持正常器官灌注是必需的。在炎症或脓毒症状态下，吞噬细胞和血管平滑肌细胞中会表达一种新的酶，导致一氧化氮不受控制地产生，这与细胞毒性作用和血管舒张有关。随机临床试验表明，给脓毒症休克患者使用一氧化氮合成抑制剂与休克缓解的发生率更高相关，且无明显不良反应。最近对一氧化氮在正常和炎症条件下不同生物学功能的发现，使得关于脓毒症休克病理生理学的新概念得以发展，并为基于一氧化氮合成抑制设计治疗脓毒症休克的新治疗策略提供了依据。
