Purpose. The aim of the present pathophysiological studies was elucidation of the feasible mechanism of spread of the blood rheological disorders from the cerebral to systemic circulation, and vice versa. Methods. The investigation was carried out in the critical care patients with the brain tissue damage related to stroke (cerebral ischemic infarcts as well as parenchymatous and subarachnoid hemorrhages). The applied diagnostic techniques provided us with valid and quantitative data revealing the degree of the red blood cell aggregability, the value of local hematocrit, and the blood plasma viscosity in the cerebral and systemic circulation. In addition, rabbits experiments were carried out for analysis of the hemorheological disorders associated with the brain damage. Results. Despite the local character of the patients primary brain damage, the hemorheological disorders were found regularly spread not only over the cerebral hemispheres, but even also the systemic circulation. Under such conditions they might cause the generalized brain tissue damage and play significant role in the subsequent damage-cascade of the whole brain. In addition, the rabbits experiments demonstrated pronounced hemorheological disorders in the cerebral cortex capillaries: increase of their numbers with RBC enhanced aggregation and blood stasis, as well as with lowering of the RBC deformability in the narrow capillary lumina. These changes befell simultaneously with increase of water contents in the cerebral tissue evidencing for edema development in the brain. Conclusion. Local cerebral hemorheological disorders might spread over the whole brain via the systemic circulation, thus promoting a generalized brain damage and being responsible for the critical state of the patients.
