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RESEARCH PRODUCT

TISSUE OXYGENATION AND TISSUE METABOLISM IN THE BRAIN CORTEX DURING PRONOUNCED ARTERIAL HYPOCAPNIA

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Publisher Summary This chapter describes the tissue oxygenation and tissue metabolism in the brain cortex during pronounced arterial hypocapnia. Acute arterial hypocapnia induced by hyperventilation leads to typical reactions in the circulation and the metabolism of the brain tissue. With a lowering of arterial CO2 tension, the cerebro-vascular resistance (CVR) increases resulting in a decrease of cerebral blood flow. The changes in CVR are a consequence of decreasing hydrogen ion and potassium ion concentrations in the perivascular space of the brain arterioles. The corresponding changes in the brain metabolism are characterized by elevated concentrations of lactate and pyruvate and an increase in the lactate/pyruvate ratio as well as an increase in the NADH level and in the NADH/NAD+ ratio in the brain tissue. The effects of arterial hypocapnia on the nerve cell metabolism and electrical activity can be attributed to the decrease in tissue PCO2. In addition, there is evidence that these changes are in part a result of insufficient blood flow because of cerebral vasoconstriction occurring during hyperventilation. Previous measurements of mean tissue PO2 and metabolites suggest that arterial hypocapnia may lead to ischemic hypoxia in small dispersed areas of the brain tissue. The decrease of PaCO2 to 2.5 kPa produced a rapid reduction of cortical blood flow. At the same time, because of the blood flow changes and in minor part to the displacement of the blood O2 dissociation curve to the left, the PO2 histograms of the cortical tissue shifted to lower values.