Hara K, Yamagami K, Nishino N, Tanaka T, Takahashi H
Department of Clinical Laboratory, Kansai Medical University, Moriguchi.
Rinsho Byori. 1998 Mar;46(3):265-70.
Recently much attention has been paid to the circulatory disturbance and peripheral vascular damage in patients with sepsis and septic shock. We intended to elucidate the interaction between nitric oxide (NO) and endothelin (ET)-1 under various pathological conditions by measuring the concentrations of NO3-, the principal metabolite of NO and immunoreactive ET-1. In cases with good prognosis after the septic shock, ET-1 was significantly higher as compared with these in sepsis without shock. In lethal cases with septic shock, these parameters were abnormally high as compared with the survived case. These levels elevated as the degree of severity progressed. When patients recovered from the septic shock, plasma ET-1 levels rapidly decreased. These results may mean that the level of the concentration of ET-1 plays a key role for prevention of the multiple organ failure even after the recovery from septic shock. The elevated level of NO3- during the initial several days in septic shock will mean that NO is acting to prevent platelet aggregation and to keep blood flow by dilating the arteries during septic shock. On the contrary, it may also be suggested that the elevated level of NO3- and ET-1 leads to the dysfunction of vascular endothelial cells and the apoptosis.
最近，脓毒症和脓毒性休克患者的循环系统紊乱及外周血管损伤受到了广泛关注。我们旨在通过测量一氧化氮（NO）的主要代谢产物NO3-以及免疫反应性内皮素-1（ET-1）的浓度，来阐明各种病理条件下NO与ET-1之间的相互作用。在脓毒性休克后预后良好的病例中，与无休克的脓毒症患者相比，ET-1显著升高。在脓毒性休克致死的病例中，与存活病例相比，这些参数异常高。随着严重程度的进展，这些水平会升高。当患者从脓毒性休克中恢复时，血浆ET-1水平迅速下降。这些结果可能意味着，即使在从脓毒性休克中恢复后，ET-1的浓度水平对预防多器官功能衰竭也起着关键作用。脓毒性休克最初几天内NO3-水平升高意味着，在脓毒性休克期间，NO通过扩张动脉来防止血小板聚集并维持血流。相反，也可能表明NO3-和ET-1水平升高会导致血管内皮细胞功能障碍和细胞凋亡。
