Role of nitric oxide in development of centralization of blood circulation upon experimental hemorrhagic shock.

Effects of a NO donor L-arginine and a non-selective NO-synthase inhibitor N(G)-nitro-Larginine methyl ester on BP, microcirculation, acid-base balance, and gas content of blood were examined on rat model of hemorrhagic shock; the substances were administered without infusion media before blood loss. Bloodletting was stopped after manifestation of marked microcirculation disorders. Inhibition of NO synthesis in response to blood loss resulted in pronounced centralization of blood circulation with microcirculation disturbances, which was accompanied by metabolic changes aggravating hemorrhagic shock. Administration of NO donor reduced the degree of circulation centralization, maintained vasodilatatory vascular tone and perfusion of vital organs, improved animal resistance to blood loss, and prolonged their lifespan. Enhanced NO generation after administration of NO donor promoted longer microcirculation maintenance, which suggests that the so-called basal level of NO is essential at early stages of hemorrhagic shock.