亚洲传统医药

Abstract: Despite modern advances in antibiotic therapy and cardiovascular support, septic shock remains a condition plagued by a high mortality rate, estimated at 40 % - 60 %. The pathogenesis of septic shock involves a complex orchestration of cytokines which lead to vasodilation, increased capillary permeability, and disturbances of metabolism. In this review, the pathophysiology of septic shock and the various isoforms of nitric oxide synthase (NOS) neuronal NOS (nNOS), endothelial NOS (eNOS) and induced NOS (iNOS) along with their possible inhibition in septic shock, are discussed. This paper also looks at the recent research on iNOS-selective inhibition in septic shock. The major clinical features of septic shock include hypotension, tissue hypoperfusion, myocardial depression, and organ failure. Current therapy focuses on early broad-spectrum antibiotic treatment, use of intravenous fluids, oxygen support and appropriate use of vasopressor and/or inotropic agents. Experimental attempts to intervene in the septic cytokine cascade hold promise, but few or none have shown definitive clinical benefit. According to the data and information available to date, we suppose that selective iNOS inhibition in septic shock may actually provide clinicians with an alternative sepsis therapy.

Key words: nitric oxide (NO), nitric oxide synthase (NOS), septic shock, inducible nitric oxide synthase (iNOS)