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.

Use of nitric oxide producer L-arginine during infusion therapy of experimental hemorrhagic shock.

Experiments on rats showed that infusion of NO precursor L-arginine before bleeding enhanced their tolerance to hemorrhagic shock. When infused after blood loss as a component of saline solution, L-arginine improved efficiency of infusion therapy for hemorrhagic shock and increased survival rate of the animals.

[Use of regulators of the nitric oxide synthesis in experimental hemorrhagic shock and its infusion therapy].

In a model of volume-controlled hemorrhagic shock in rats bolus injection prior to hemorrhagic of non-selective inhibitor of the nitric oxide synthases--N-Nitro-L-Arginine at the dose 250 mg/kg promotes considerable blood flow redistribution and rapid death of animals. However the donor of nitric oxide--L-Arginine (300 mg/kg) enchances stability of animals in hemorrhagic shock. Infusion of L-Arginine (300 mg/kg) with physiological salt solution after bleeding restored cardiac function and microcirculation in the serous membrane of the small intestine of rats.

Effect of selective inhibitors of nitric oxide synthesis on the course of experimental hemorrhagic shock.

Selective inhibitors of NO synthesis (derivatives of lysine, ornithine, and isothiourea) increased the efficiency of infusion therapy for experimental hemorrhagic shock in rats. These changes were related to improvement of cardiac function (increase in stroke volume, cardiac output, and left ventricular efficiency). Among the three inhibitors, N5-(1-iminoethyl)-L-ornithine dihydrochloride was most potent on this experimental model.

[Effect of dinitrosyl iron complex with glutathione as a nitric oxide donor on blood circulation in healthy animals].

It has been shown that the hypotensive action of the nitric oxide donor, the dinitrosyl complex of iron with glutathione, on the organism of healthy rats, which is caused by a decrease in the general peripherical immunity, does not impair the microcirculation and is accompanied by an enhancement of the contractile activity of the myocardium. In hypotension caused by the dinitrosyl iron complex, neither the tension of oxygen and nitrogen in the blood nor its basic-acidic status changes. Thus, the possible inhibitory action of this complex on some enzymes and proteins in the animal organism does not affect the functioning of the heart, vessels, and blood.