STUDIES ON THE CORONARY CIRCULATION

Abstract
To study the factors involved in the formation, distribution and disposal of lactic acid in the body, analyses were made of simultaneous samples of arterial and of coronary venous blood of the beating heart in situ. Arterial blood pressure, heart rate and, in most experiments, respiration and coronary volume flow measurements were recorded. In 226 of 230 pairs of samples in 16 dogs under a variety of experimental conditions, coronary venous blood contained less lactic acid than the corresponding sample of arterial blood. Faradic stimulation of the vagus in 13 observations on 9 dogs for about 2 min. reduced blood pressure, heart rate and coronary sinus volume flow (recorded in 11 experiments) during the stimulation. There occurred a corresponding decrease in minute absorption of lactic acid from an average of 6.0 mgm. to 3.2 mgm. per min. The reduced gradient of inward movement of lactic acid from blood to muscle is explained by increased production of lactic acid in the muscle because of impaired oxidations induced by the fall in coronary volume flow of blood. Despite the lowered gradient, there was observed an increased difference (bearing an inverse re-lationship to the velocity of flow) in lactic acid content of arterial and venous blood. Faradic stimulation of the stellate ganglion for about 2 min. in 13 observations on 8 dogs was followed by increased blood pressure, heart rate and coronary volume flow (recorded in 10 experiments) during the stimulation. A corresponding and uniform decrease in absorption per unit volume flow of blood was observed. Minute absorption decreased in 5 experiments, increased in 4, and remained the same in one. An average of all experiments indicated virtually no change in minute absorption. Moderately effective injections of pitressin caused diminished heart rate, a moderate fall in coronary volume flow and slightly increased minute absorption. Arterial venous differences increased slightly. More effective injections of pitressin, with considerable reductions in coronary-volume flow resulted in greatly decreased minute absorption, due to the reduced supply of O to the cardiac muscle. In 4 experiments the falling gradient of lactic acid absorption gave way to an outward flow of lactic acid from muscle to blood. The heart normally absorbs lactic acid from the blood. This absorption is inde-pendent apparently of the level of concentration in arterial blood and continues to obtain even during considerable reductions in coronary volume flow of blood, although the rate of absorption is diminished. With extensive impairment of oxidations lactic acid may form to such an extent in the cardiac muscle as to diffuse into the blood.

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