Abstract
Blood in its passage through the brain loses oxygen and glucose at relatively high rates, the amount of oxygen disappearing being approximately equivalent to the amount of glucose consumed, calculating on the basis that the sugar is completely oxidized. The respiratory quotient of brain in vivo is unity. These facts point to the dominance of carbohydrate oxidation in brain respiration in vivo and are similar to those found in studies of brain in vitro.
Various factors influence glucose oxidation in brain, e.g. changes in the ionic environment of the cells, vitamin B1, or the presence of narcotics. The latter bring about inhibitions of glucose oxidation in brain tissue which may in most cases be shown to be reversible in vitro. Glucose is not only important for the maintenance of respiration of brain but for enabling certain synthetic processes to occur. One of these is the formation of acetylcholine whose physiological significance is now well known and whose synthesis seems to be confined to the nervous system. This synthesis depends not only on the presence of glucose but on that of oxygen. The influence of glucose has been observed also in investigations on cortical potentials.
An important feature of the nerve cell is its vulnerability to the lack of oxygen. Reversibility depends on the degree and duration of the anoxæmia.
During insulin shock treatment studies of brain in vivo show lowered oxygen consumption and glucose utilization, these depending on the degree of hypoglycæmia. In cardiazol treatment, in vivo studies show that the oxygen content of the blood may fall to 42%. During the convulsion there is a greatly lowered arterial and venous blood-flow through the brain and cerebral anæmia becomes a marked feature. In narcosis treatment both in vitro and in vivo studies show a diminished ability of the brain to consume oxygen.
It is suggested that the most significant facts to be taken into account are (1) the importance of glucose and oxygen for the metabolism and function of the nervous system, (2) the vulnerability and varying sensitivities of nerve cells to lack of oxygen and glucose, (3) the occurrence of varying degrees of cerebral anoxæmia in narcosis, insulin and cardiazol treatments.
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Selected References
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