DELAYED HYPERGLYCEMIA AND INTRACELLULAR ACIDOSIS DURING FOCAL CEREBRAL-ISCHEMIA IN CATS

The effects of hyperglycemia on permanent focal brain ischemia is cont roversial; its effects on the size of the infarct are variable accordi ng to experimental conditions. In this study, nuclear magnetic resonan ce (NMR) spectroscopy was used to assess brain pH and high-energy phos phate metabolites after focal middle cerebral artery (MCA) ischemia in hyperglycemic and normoglycemic cats. Sixteen adult cats underwent (M CA)occlusion under general anesthesia and nuclear magnetic resonance P -31 spectroscopy to assess intracellular brain pH and energy metabolit es throughout permanent ischemia. Animals were treated two hours after the onset of ischemia with either saline or glucose perfusions. Signi ficant hyperglycemia (488 vs 105 mg/100 mi) was achieved in the experi mental group. The response to hyperglycemia was dependent on the initi al characteristics of the infants. A distinct pattern of phosphocreati ne/inorganic phosphate recovery within 20 minutes of ischemia predicte d a small infarct size. The addition of hyperglycemia did not affect a cidosis, 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 intracel lular pH during the ischemic period (5.45 vs. 6.25, p = 0.25). These d ata support the theory that the response to hyperglycemia is very depe ndent on the initial metabolic state of the injured brain. This state can be predicted by early P-31 spectroscopy data, which may, in turn, prove to be a useful marker for recoverable ischemic deficit in the ce rebral region of interest.