Abstract
The effects of blood glucose on brain tissue metabolism and blood flow were studied in 3-hour incomplete cerebral ischemia induced by bilateral carotid ligation in spontaneously hypertensive rats (SHR). Prior to cerebral ischemia, blood glucose levels were varied by intraperitoneal injections of 50% glucose (hyperglycemia), 8% NaCl (normoglycemia) or insulin + 8% NaCl (hypoglycemia). Lactate, pyruvate and adenosine triphosphate (ATP) concentrations in the supratentorial brain frozen in situ were measured by the enzymatic method. Local cerebral blood flows (CBF) in the parietal cortex and thalamus were measured by the hydrogen clearance method before and after carotid ligation. Brain metabolites and blood flows were also determined in sham-operated, non-ligated SHR with various blood glucose levels.
Supratentorial lactate in ischemic brain increased more greatly in hyperglycemia (34.97±1.29 mmol/kg) than normoglycemia (23.43±3.13 mmol/kg) (p<0.005), although cerebral ATP decreased to a similar extent in both groups. In contrast, cerebral lactate as well as pyruvate was less markedly increased in hypoglycemia (7.20±1.54 mmol/kg) as compared with those in normoglycemia (p<0.001), but reduction of ATP was greater in the former (0.45±0.05 mmol/kg) than the latter (1.04±0.25 mmol/kg), of its difference being significant (p<0.05). In non-ischemic brains, there were no differences of cerebral metabolites among three glycemic groups of animals. Cortical CBF was pronouncedly decreased to approximately 10% of a pre-ligated value immediately after, and further to less than 1% at 3 hours after carotid ligation, nevertheless blood glucose levels. Thalamic CBF was similarly but less markedly reduced during cerebral ischemia in all animals.
It has been reported that hyperglycemia is vulnerable to brain metabolism in complete cerebral ischemia, presumably due to hyperglycemia-induced lactic acidosis of the brain. In complete ischemia as demonstrated in the present study, however, brain energy metabolism was maintained in hyperglycemia as much as normoglycemia, although an increase in lactate was significantly greater in the former. It was indicated that increased blood glucose level might be beneficial rather than vulnerable to brain metabolism in incomplete ischemia. On the other hand, hypoglycemia of even moderate degree caused more severely impaired energy metabolism of the brain because of an insufficinet supply of substrate to ischemic brain.
