OXIDATION OF PYRUVATE AND GLUCOSE IN BRAIN SUSPENSIONS FROM ANIMALS SUBJECTED TO IRREVERSIBLE HEMORRHAGIC SHOCK, CARBON MONOXIDE POISONING, OR TEMPORARY ARREST OF THE CIRCULATION—A STUDY OF THE EFFECTS OF ANOXIA

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Abstract
The respiratory metabolism of cerebral biopsy specimens homogenized in Ringer''s soln. was detd. mano-metrically after induced anoxia of irreversible hemorrhagic shock (dogs, blood pressure 30 mm. Hg for 2-3 hrs.); CO hypoxia (dogs, 75 to 85% HbCO for 50-70 mins.); and temporary (4.5-9 mins.) circulatory arrest (cats). Biopsies were taken one to several wks. before the induction of anoxia, immediately thereafter, and/or, occasionally, following recovery from the reversible types of anoxia. A method was devised for computing the respiratory activity of gray matter relative to the water content of biopsy specimens of unknown composition and the mean values for water content and respiratory activity in pure gray and white matter. In expts. with pyruvate as substrate, measurements were made both with and without added thiamine-HC1 to test whether anoxia produced a critical thiamine deficiency. Control expts. on brain suspensions from pigeons with severe vit. B1 deficiency showed striking increase in respiration after addition of thiamine. In some but not all of the brain samples from the animals exposed to circulatory arrest, lowered rates of O2 consumption with pyruvate as substrate and diminished respiratory rates and quotients with glucose as substrate were found. In CO hypoxia and in hemorrhagic shock the respiration of the brain remained normal. The addition of thiamine was without effect in all 3 types of induced anoxia. It is concluded that a destruction of respiratory enzymes or a critical deficiency of co-enzymes in the brain is not a primary consequence of anoxia nor do such factors account for the development of irreversible functional and histo-logic alterations that may follow anoxia.

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