Effect of increased plasma levels of glucose, adrenaline, and angiotensin upon glucose metabolism of totally ischemic and normally perfused rat brain]

Tracer kinetic studies on the effect of i.v. infused adrenaline and angiotensin, and a hyperglycemia induced by glucose application, upon glucose metabolism of the rat brain under ischemic and normoxic conditions are reported. in the ischemic brain, the initial glycolytic rate proved dependent on the glucose content being kept at various levels by glucose administration or hormone infusion prior to the onset of ischemia. The typical saturation kinetics revealed a maximal glucose conversion only from a definite initial content of brain glucose, being equivalent to a glucose level of approximately 13 mumole/ml in plasma, and appeared to depend on the presence of glucose in the cellular space. The early cessation of anaerobic lactate formation even with high glucose in the cellular space. The early cessation of anaerobic lactate formation even with high glucose depot in the brain tissue is referred to inhibition of glycolytic key enzymes by increasing tissue azidosis. The aerobic glucose conversion, as calculated from the Cglucose flux in amino acids associated with the citrate cycle was unaffected by the cerebral glucose content (hyperglycemia by hormone or glucose application). During glucose infusion the cerebral levels of NH3, total NH2 and glutamine rose; the Cglucose flux into aspartate and glutamine was increased and almost proportionally reduced in glutamate and gamma-aminobutyrate. These flux shifts are interpreted as a switching of C-chains from pyruvate owing to increased CO2 fixation, and as a biochemical correlate of an increased irritation level of the experimental animals.