A study was made to determine what biochemical changes were involved in the slowing of the rat heart rate during thiamin deprivation, pyrithiamin or oxythiamin treatment. The appearance of bradycardia during progressive thiamin deficiency was shown to be related to the reduction in myocardial enzymatic activity of pyruvate (PDH) and 2-ketoglutarate (2-KGDH) dehydrogenase, and not due to inanition alone since pair-fed control rats did not show bradycardia until the agonal stage. Bradycardia was not the result of reduced energy since CP, ATP, ADP, and AMP levels remained normal even though PDH and 2-KGDH activity dropped to 20% of normal by the fourth week of thiamin deficiency. Pyrithiamin treatment resulted in a 46% increase in CP. The in vivo bradycardia persisted in the in vitro isolated perfused heart and was not the result of elevated blood pyruvate, lactate or H+. Abnormalities of the ECG of thiamin deficient rats did not occur until two weeks after the appearance of bradycardia, suggesting a sinus origin for the slower heart rate.
College and Department
Plant and Wildlife Sciences
BYU ScholarsArchive Citation
Sutherland, D. James B., "The effects of thiamin deficiency and thiamin antagonists on cardiac function in the rat" (1973). Theses and Dissertations. 7897.
Vitamin B1 deficiency; Cardiovascular system; Rats