ALTERATIONS IN BLOOD LACTIC ACID AS A RESULT OF EXPOSURE TO HIGH OXYGEN PRESSURE

Abstract

Dogs anesthetized with morphine and urethane were exposed to Oa at pressures of about 5 atmospheres, and ensuing alterations in blood lactic acid (LA) determined. Periods of exposure to the increased pressure were usually of about 30-min. duration and were preceded and followed by administration of O2 at one atmosphere. Decompression was carried out in stages, and over such periods of time as to avoid effervescence. The preliminary exposure to O2 at one atmosphere was frequently attended by a slight drop in LA content of the blood. Subsequent breathing of O3 at pressures of about 5 atmospheres usually was attended by an increase in blood LA. Of 18 expts. 15 showed an increase in blood LA while 4 showed no appreciable change. Recovery from the LA increase was practically complete in 6 expts. on decompression. Of the others, 6 showed only partial recovery and in 3 more the LA continued to increase during and subsequent to decompression. Respiratory minute volume was increased during exposure to high O2 pressure in all expts. except one. Evidence is presented to show that the LA increase was not due to increased activity of the respiratory muscles. Cellular damage resulting from high O2 pressure was considered as a possible factor contributing to the LA increase in the blood. Intracellular acidity arising from a broken coordination of the dual function of the Hb is discussed as a possible indirect cause for the LA increase. The increased intracellular acidity might give rise to an augmented production of LA by lowering of oxidations. It might also cause a shift in LA from the interior of the cell to the blood. A possible enzymatic control of LA removal is suggested. High O2 pressure might have a toxic effect on the enzymes involved, thereby accounting for the accumulation of LA during exposure of the animal to high O2 pressure.