Delayed hyperglycemia and intracellular acidosis during focal cerebral ischemia in cats.

The effects of hyperglycemia on permanent focal brain ischemia is controversial; its effects on the size of the infarct are variable according to experimental conditions. In this study, nuclear magnetic resonance (NMR) spectroscopy was used to assess brain pH and high-energy phosphate metabolites after focal middle cerebral artery (MCA) ischemia in hyperglycemic and normoglycemic cats. Sixteen adult cats underwent (MCA) occlusion under general anesthesia and nuclear magnetic resonance 31P spectroscopy to assess intracellular brain pH and energy metabolites throughout permanent ischemia. Animals were treated two hours after the onset of ischemia with either saline or glucose perfusions. Significant hyperglycemia (488 vs 105 mg/100 ml) was achieved in the experimental group. The response to hyperglycemia was dependent on the initial characteristics of the infants. A distinct pattern of phosphocreatine/inorganic phosphate recovery within 20 minutes of ischemia predicted a small infarct size. The addition of hyperglycemia did not affect acidosis, infarct size, or metabolite ratios in these animals. The lack of phosphocreatine/inorganic phosphate recovery within 20 minutes of ischemia was predictive of an eventual large infarct. In these animals, the delayed addition of hyperglycemia significantly lowered intracellular pH during the ischemic period (5.45 vs. 6.25, p = 0.25). These data support the theory that the response to hyperglycemia is very dependent on the initial metabolic state of the injured brain. This state can be predicted by early 31P spectroscopy data, which may, in turn, prove to be a useful marker for recoverable ischemic deficit in the cerebral region of interest.