Nitric Oxide (NO) is synthesized endogenously from the guanidion group of the amino acid arginine in a reaction catalyzed by nitric oxide synthase. It is involved in the regulation of blood pressure through the maintenance of vasodilator tone by NO synthesized in vascular smooth muscle cells. Evidence suggests that the hypotensive actions of lipoploysaccaride may be due to increased synthesis of NO, as L-NG-methyarginine hydrochloride, a competitive inhibitor of nitric oxide synthase, reverses they hypotension induced by administration of LPS. Although there is ample in vitro evidence that nitric oxide synthase is induced by sepsis, leading to increased tissue levels, there is no evidence that nitric oxide synthase is induced by sepsis, leading to increased tissue levels, there is no vivo data demonstrating a relationship between increased NO production and hypotension in septic patients. We propose to test the hypothesis that a rate of production of arginine and its conversion to nitric oxide is increased in hypotensiveseptic patients, and that administration of L-NG-methyarginine hydrochloride. In a comparison of 5 hypotensiveseptic patients and 8 controls, we found that the hypotensiveseptic patients had a slower argininine flux and a slower rate of conversion of arginine to NO. This refutes the theory that hypotension in hypotnsiveseptic pateints is due to increased NO production.
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