THE REGULATION OF RESPIRATION

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Abstract
As an index to lactic acid metabolism in the brain of an intact animal, simultaneous lactic acid determinations were made on arterial blood supplying the brain and on venous blood returning from the brain with a few volume flow measurements. In 12 of 29 experiments, venous blood from either the superior sagittal sinus, or the external or the internal jugular vein, contained initially less lactic acid than arterial blood, indicating a movement of lactic acid from the blood into the tissues. In 10 experiments, arterial and venous lactic acid contents were at the same level. In 7 experiments venous blood contained initially more lactic acid than arterial blood, indicating an outward movement from the brain tissue into the blood. Impairment of oxidations in the brain by injection of NaCN, partial or complete occlusion of the cerebral blood supply, and diminished pulmonary ventilation, resulted in an increased content of lactic acid in venous blood over that of arterial. Injection of NaCN in one experiment caused a relatively increased production of lactic acid in the brain of over 250%. In another experiment, a fall in blood pressure resulted in a decrease in absorption of lactic acid from arterial blood to 24.5% of the initial rate, with partial recovery to 74% of the initial rate. A temporary reduction of arterial blood supply in another experiment caused a 50% reduction of lactic acid absorption from arterial blood. It is believed that, with normal oxidations in brain tissue, lactic acid is absorbed from the arterial blood and utilized by the brain cells. With impaired oxidations there occurs an excessive production of lactic acid in brain cells with an outward diffusion into the blood stream. The analogy between lactic acid metabolism of muscle and that of the brain is believed to be more firmly established, while the relationship to the chemical control of respiration receives support.

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