No description available.

The determination of total thiamin, free thiamin, thiamin di phosphate (TDP) plus thiamin triphosphate (TTP), and total α- hydroxyethylthiamin (HET) levels in rat brain in control, deficient, oxythiamin- (OTH) and pyrithiamin- (PTH) treated rats was accomplished. It was found that the TDP + TTP/thiamin ratio observed in the thiamin-deficient, OTH- and PTH-treated rats was constant and did not differ from the ratio observed in the control rat brains. The brain levels of TDP + TTP decreased to 39% and 12% of the control thiamin levels in deficient and PTH-treated rats respectively. The brain HET and TDP + TTP levels of the OTH-treated rats were not significantly different from the controls. The HET levels in the PTH rats decreased significantly ( α = 0.005) by treatment day 4 and decreased to one-seventh of the control values in the terminal stages. A significant drop in the HET levels from the control levels was interpreted to mean that the pyruvate utilization was significantly impaired in the brain.

No description available.

Thesis (Ph. D.)--State University of New York at Binghamton, Department of Psychology, Behavioral Neuroscience, 2008. / Includes bibliographical references.

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.

Thesis (M.S.)--State University of New York at Binghamton, Department of Psychology, 2009. / Includes bibliographical references.