• S Wang, G Hao, X Shen, and D Jing.
• Department of Pathophysiology, West China University of Medical Sciences, Chengdu, China.
• Chinese Med J Peking. 1998 Mar 1; 111 (3): 242-7.

ObjectiveTo examine the relationship between the profound hypotension in endotoxic shock and the dynamic changes of nitric oxide (NO) and endothelin-1 (ET-1), so as to figure out which of the NO or ET-1 was more involved in the pathogenesis of endotoxic shock. And to investigate whether an offset of their opposite vasoactive effects would occur during endotoxic shock.Methods24 rabbits were anesthetized and instrumented for recording hemodynamics. Endotoxin (E. coli 026: B6, 600 micrograms/kg) was bolus injected intravenously and the animals were randomly divided into four groups. Group I was control without any more intervention, and Group II, III, IV received bolus injections of L-NMA (10 mg/kg), phosphoramidon (2 mg/kg) or dexamethasone (2 mg/kg) respectively at 30 min post-endotoxin. Plasma NO3-, ET-1 and hemodynamics were measured at regular intervals. Their relationships were compared and analysed.ResultsPlasma ET-1 achieved its peak level at 60 min post-endotoxin, and then waned. Plasma NO3- started rising at 120 min post-endotoxin, then progressive increase continued till the last measurement at 180 min post-endotoxin. The decrease of blood pressure was significant at about 120 min post-endotoxin and further went down until death. The changes of hemodynamics and NO showed a quite close temporal correspondence between the increase of NO and the decrease of blood pressure. L-NMA and phosphoramidon obviously reduced the plasma levels of NO and ET-1 to below their respective baseline levels, and showed transient effect of increase on blood pressure. Soon afterwards, however, the status of hemodynamics was aggravated. Dexamethasone just inhibited the excessive increase of NO and ET-1 during endotoxic shock without interfering their baseline levels and showed most beneficial effects on hemodynamics.ConclusionsBoth NO and ET-1 increase during endotoxic shock, but only the increase of NO has a close temporal correspondence with the decrease of blood pressure. It suggests a more important role of NO in pathogenesis of endotoxic shock. The increase of NO and ET-1 is different in time-process, which indicates that an offset of their opposite vasoactive effects would not occur. Intreference against the increase of NO and ET-1 during endotoxic shock is most beneficial when their baseline levels are maintained.

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