The induction and reversibility of cerebral acidosis in thiamine deficiency

Abstract

Regional cerebral pH was determined autoradiographically using carbon 14-labeled dimethyloxazolidinedione in normal rats, following various durations of thiamine deficiency and replenishment with thiamine when the clinical sequelae of the deficiency appeared. In our model the clinical sequelae of thiamine deficiency (opisthotonus) appeared on the average on day 18. Regional cerebral pH on day 12 was comparable to that in controls and ranged between 7.02 ± 0.03 and 7.09 ± 0.03 (mean ± SEM) in gray matter structures. On day 14 the pH in the inferior colliculus was 6.85 ± 0.08 and relative acidosis also appeared in thalamic structures. At opisthotonus the pH was 6.48 ± 0.17 in the mamillary body, 6.43 ± 0.14 in the vestibular nucleus, and 6.36 ± 0.14 in the medial dorsal nucleus of the thalamus (p < 0.01). One dose of thiamine replenishment at this stage transiently raised the pH in the inferior colliculus to 7.25 ± 0.19 and in the medial dorsal nucleus to 7.20 ± 0.13 (p < 0.01). Cerebral regions showing significant acidosis during thiamine deficiency coincided largely with those known to be histologically vulnerable and those previously reported to show a focal rise in local cerebral glucose utilization between days 11 and 14 of thiamine deficiency. This focal acidosis shown to occur in thiamine deficiency may be one mechanism contributing to the selective histological vulnerability in this model.