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In experiments on rats it was shown that injection to rats before hemorrhage of analeptic corasol or prior injections during three days of the inhibitory mediator sodium oxybutyrate decrease individual resistance of the respiratory and circulatory systems (arterial blood pressure, cardiac output, organ portal blood flow) to posthemorrhagic hypoxia. Injection to animals before the hemorrhage of GABA-A antagonist picrotoxin significantly raises individual resistance to massive bleeding. Individual resistance to acute hemorrhage correlates with individual sensitivity of cardiovascular and respiratory systems to corasol.

A marked fall in arterial blood pressure, organ blood flow rates and tissue perfusion in the liver, kidneys and brain was registered by ultrasound and laser Doppler flowmetry in rats with low (LR) and high resistance (HR) to circulatory hypoxia (average life spans less than 1.5 h and more than 3 h were 42 and 58%, respectively) at the end of acute massive hemorrhage. In the posthemorrhagic period organ hemodynamics and microcirculation showed a tendency to further decrease in LR rats. In HR rats blood flow in hepatic, renal and common carotid arteries were restored for a while up to 115-120%, 85-90% and 60-65%, respectively, following bleeding arrest. At this new posthemorrhagic level the brain flow was actively maintained in the compensatory phase of the posthemorrhagic period due to autoregulatory changes in the carotid resistance. Such a peculiar reaction of the brain blood vessels in HR rats is considered as an adaptive response protecting the brain during massive hemorrhage under severe tissue hypoxia against autoreperfusion and reoxygenation-induced damage.

Monitoring by ultrasonic and laser Doppler flowmetry and biomicroscopy demonstrated that rats highly resistant to acute blood loss differ in principle from rats with low resistance by the life span, pattern of changes in arterial pressure, organ hemodynamics, and microcirculation. The pumping function of the heart is intact till the end of life in all highly resistant and in 65% poorly resistant rats. After arrest of massive hemorrhage, 35% poorly resistant animals develop low cardiac output syndrome. Poorly resistant rats with severe posthemorrhagic hypotension represent a risk group in need of special pathogenetic therapy.

Ultrasonic and laser doppler flowmetry, biomicroscopy were used in the study of systemic hemodynamics, microcirculation, blood flow in the brain, liver, kidneys and inferior limb in rats varying by resistance to acute blood loss. In the course of bleeding both high- and low-resistant rats (HRR, LRR) had the same decline in blood pressure, blood flow rate and tissue perfusion. When blood loss stopped. HRR developed relative compensation of the above parameters followed by irreversible fall. Posthemorrhagic recovery of these hemodynamic parameters in LRR was not observed. All the LRR showed persistent generalized constriction of hepatic, intestinal and renal microcirculation. Pumping performance of the heart continued to death in all HRR and in 65% of LRR. After stop of hemorrhage, 35% of LRR developed minor cardiac ejection syndrome which was followed by death within 30 min.

Systemic hemodynamics and hepatic macro- and microcirculation (ultrasonic technique, biomicroscopy) were studied in intact rats and rats with acute massive hemorrhage after intravenous administration of the calcium antagonists verapamil and nifedipine. It was shown that verapamil deteriorated the posthemorrhagic period in rats with decompensated hemorrhage which was associated with the specific features of the calcium antagonist on the cardiovascular system of intact rats (decrease of blood pressure, total peripheral resistance, heart power). In rats with compensated hemorrhage verapamil and nifedipine blocked the development of posthemorrhagic liver microcirculatory disturbances, improved hepatic tissue perfusion and stabilized portal organ blood flow velocity on the longer period than in the untreated group of rats.

Using the method of contact luminescent biomicroscopy of the liver and intestine coupled with the measurement of systemic blood pressure by micromanometer and ultrasonic registration of blood flow velocity in portal vein and hepatic artery it has been established that in rats with acute decompensatory hemorrhage fragments of ACTH (1-24) and (4-10) improve the state of portal macro- and microcirculation and increase the life span 2-3-fold. ACTH does not influence the dynamics of acute compensatory hemorrhage and the development of the posthemorrhagic microcirculatory disturbances (local microstases, microthromboses, erythrocyte aggregation).

The experiments on rats using the method of contact luminescent biomicroscopy coupled with the ultrasonic measurement of systemic blood pressure and blood flow velocity in the portal vein and hepatic artery have revealed that portal micro- and macrocirculation reflects the degree of efficacy of acute hemorrhage treatment with autoblood. Autoblood infusion in animals with compensatory type of posthemorrhagic period restored systemic blood pressure and blood flow velocity in the portal vein and hepatic artery, promoting the development of erythrocyte aggregation and local microcirculation disturbances in the central zone of hepatic functional elements.

Fluorescent contact biomicroscopy has shown the presence of the protein permeability gradient in postcapillary and venular parts of the microvascular bed of the rat mesentery and stomach. Albumin and globulin that egressed into extravascular spaces were reabsorbed by lymphatic microvessels. Fluorescent protein was also detected in the form of golden granules in the endothelium of venules and in pericytes adjacent to the venular parts. The data obtained are discussed in the light of the role of venular and lymphatic microvessels in transcapillary exchange at the level of the functional organ element.

Using the method of contact luminescent biomicroscopy of the liver and the intestine coupled with the ultrasonic measurement of systemic blood pressure, blood flow velocity in the portal vein and hepatic artery it has been established that in rats with acute decompensatory hemorrhage naloxone increases blood pressure and improves the state of protal macro and microcirculation only after i. v. injection of large dose (5 mg/kg). Naloxone does not influence the dynamics of acute compensatory hemorrhage and the development of the posthemorrhagic microcirculatory disturbances (local microstases, microthromboses, erythrocyte aggregation).