EFFECTS OF HIGH OXYGEN TENSIONS UPON THE CARBON DIOXIDE PRODUCTION OF SKELETAL MUSCLE AND OTHER TISSUES OF THE FROG

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Abstract
High O2 pressure (8-35 atm.) causes a decrease in the CO2 output of isolated frog sartorii; the higher the O2 pressure employed, the sooner the decrease occurs. That the O2, and not the pressure, is responsible for the decrease is evident from the following two facts: Increasing the pressure with N2 caused no decrease in CO2 production. When O2-N2 mixtures were used, the decrease in CO2 production was related to the partial pressure of O2 rather than to the total pressure. Upon acidification, an O2-poisoned muscle freed an amt. of CO2 equal to only 11 % of the deficit in CO2 output which had been incurred by the muscle during its subjection to high O2 pressure. This indicates that the lowering of the CO2 output of a muscle in the presence of a high O2 tension cannot be attributed to the retention of CO2 by buffers in the muscle. In addition, the accumulation of acid metabolites in an O2-poisoned muscle is suggested by the fact that the preformed CO2 per gram of this muscle was somewhat lower than that of the control muscle. "Activity" CO2 production induced by KC1 is inhibited by high O2 pressure. Loss of the ability to twitch precedes alterations in the appearance of the O2-poisoned muscles. Each of these changes is a function of the product of O2 tension and time. That the change in the CO2-producing system is reversible, at least, in part, is indicated by the fact that following decompression, CO2 production rises to a point above the initial rate. The fact that the second compression, in two instances, caused a quicker decrease in CO2 output than the first compression points to the existence of a cumulative effect in the action of high O2 pressure upon some CO2-producing system of muscle. High O2 pressure appears to cause an increase in CO2 production immediately after compression. Kidney, liver, skin, lung and nerve also respond to high O2 pressure by decreased CO2 production. The rate of CO2 output falls to 50% of the initial rate more quickly in nerve than in any other tissue. Early increases in rate appeared only in kidney, lung and nerve. Apparatus is described which makes possible the measurement of the CO2 production of a tissue during its exposure to high pressure of O2 or N2.

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