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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.

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.