Abstract
THE work of Peters1 and his collaborators has shown that abnormal amounts of lactic and pyruvic acid accumulate in the brain of the polyneuritic pigeon. Further evidence of the Oxford school has demonstrated that the brain tissue of such polyneuritic pigeons exhibits a lowered oxygen consumption in the presence of either pyruvic or lactic acid. The addition of vitamin B1 in vitro to such tissue restores the oxygen uptake to a large extent. Other workers2 have also pointed out the presence of excessive amounts of lactic acid in the tissues of the vitamin B1 deficient animal. This emphasis on the lactic acid theory of the vitamin B1 syndrome led Drury, Harris and Maudsley3 to suggest that the bradycardia found by them in vitamin B1 deficient rats was due to the excessive accumulation of lactic acid in the heart. No direct evidence was brought forward to support this theory, although the results of Birch and Harris4 showed that the severity of the bradycardia went parallel with the lactic acid level in the blood.
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