Abstract
Endothelial derived relaxation factor has recently been identified as the free radical nitric oxide.1 Nitric oxide is produced by endothelial cells, hepatocytes, Kupffer cells, neutrophils, and macrophages. All of these cells utilize L-arginine as a substrate for nitric oxide production2 and each has been documented as having a role in the development of septic and/or endotoxic shock. Recent evidence has suggested that nitric oxide may be a significant mediator in the acute hypotension, cardiovascular dysfunction, and tissue injury associated with septic shock; therefore, inhibition of nitric oxide has been proposed as a potential therapeutic treatment in septic patients.3 Our goal was to determine if the inhibition of nitric oxide synthesis attenuates the cardiovascular, metabolic, and pathological responses induced by endotoxin in the conscious rat. To accomplish this, NG-monomethyl-1-arginine (L-NMMA), an inhibitor of both Ca2+-dependent and Ca2+-independent nitric oxide synthesis, was utilized.
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