| Abstract: | The concepts about physiological mechanisms of oxygen transport to the brain have recently changed substantially. Precise data on the capillary blood flow rate, on a substantial dispersion of corresponding values, on the influence of the capillary blood flow rate on pO2 in the capillaries and tissues have evolved. Krog's paradigm about an exclusive role of capillaries in the gas exchange between the blood and tissues amounting to almost 100 years was abandoned. All these data also changed the concepts about the development of various types of hypoxia in the brain tissues. The study of pO2 in the brain at normoxia showed that pO2 exhibits the fluctuations from 1-2 to 80-85 mm Hg. This means, in particular, that hypoxic phenomena take place in the normal healthy brain. During hypoxia the mass adhesion of leukocytes to the walls of microvessels was shown to hamper the capillary blood flow and can become one of the reasons for the death of the brain during hypoxia. The brain hypoxia is not an occasional pathologic process. It exists in an intact brain owing to physiological fluctuations of pO2 in various microregions of the brain. It occurs during various physiological states in the norm and also during various illnesses associated with the changes and disruptions in the oxygen transport. The final stage of hypoxia is the destruction of the cells. The development of this process and its particular reasons are nowadays the subject of multiple physiological and biochemical studies. Certain changes are introduced into modern ideas about the reasons for the degradation of the nervous cells upon hypoxia. The degradation of the neurons during hypoxia or anemia is postulated to be associated not only with the cell generation of active forms of oxygen (AFO), but also with the energy deficiency. This means a deficient synthesis or a complete absence of ATP in a cell during hypoxia, anemia, and ishemia. |
