Ischemic brain edema as a complication of decompensated hypovolemic shock.

Four-hour arterial hypotension (decompensated phase) in dogs caused by acute blood loss, when the level of arterial pressure of 40 mmHg was maintained beginning from the 2nd and 3rd h by intra-arterial intermittent blood transfusion is an adequate model for reproducing a moderate ischemic edema of the brain. Pronounced hypoperfusion and considerable disturbances in blood fluidity testified to greater severity of hypoxic and hemorheological disturbances in the microvessles of the brain in decompensated animals than in their compensated counterparts. The formation of a brain edema is based on disturbed fluid circulation closely related to the structural pathology of the organelle membranes of the cells of the nervous and vascular tissues. The pathology of the organelle membranes of the cell elements of the vascular tissue leads to direct diffusion of the liquid through the vessel wall into the brain parenchyma thus disturbing intertissue relations. The pathology of the cell element membranes of the nervous tissue (neurocytes, oligodendrogliocytes and astrocytes) leading to intracellular disturbance of fluid circulation makes its contribution to changes in inter-tissue interactions. Brain hyperhydration was revealed only in animals that had sustained decompensated hypovolemic shock.