| Abstract: | The paper describes differences of hypoxic and circulatory hypoxias (i.e. brain ischemia) which cause decreases not only in the supply of O2, but in the delivery of glucose and other oxidation substrates and in venous return, which is attended by the accumulation of metabolic products in the brain tissue. It also considers the mechanisms of primary and secondary brain ischemia occurring with decreased cerebral circulation due to breakdown of cerebral blood flow autoregulation at its lower and upper borders to develop cytotoxic or vasogeneous brain tissue edema with possible compression of the microcirculatory bed in the latter case. Emphasis is laid on the significance of autoimmune reactions occurring with the impaired blood-brain barrier due to different types of cerebral circulatory disorders, which gives an insight into the cause of progressive damage to the brain in some cases despite its single damage. The paper outlines current therapies for brain ischemia, including those that exert effects on metabolic disturbances and neurosurgical reparative operations. In conclusion, the paper considers a new nontraditional way of increasing collateral CBF by decreasing blood flow pseudoturbulence with special high molecular-weight linear polymer solutions by the Thoms-effect method (1948). The prospects for using this approach in patients with brain ischemia are substantiated by a number of the established facts: 1) the above patients have higher hemodynamic blood flow resistance which may be corrected by adding a polymer solution into the sample in in vitro tests; 2) there was an inverse relationship of the intrinsic plasma concentrations of high molecular-weight fragments of DNA and hemodynamic resistance to the changes in plasma DNA properties in stroke patients. |
