EFFECT OF HYPERGLYCEMIA ON REPERFUSION-ASSOCIATED RECOVERY OF INTRACELLULAR PH AND HIGH-ENERGY PHOSPHATE AFTER TRANSIENT CEREBRAL-ISCHEMIA IN GERBILS

Hyperglycemia increases cerebral damage after transient cerebral ische mia. This study used in vivo P-31 nuclear magnetic resonance spectrosc opy lo determine the relationship of intracellular tissue acidosis and delayed recovery of brain high-energy phosphates to increased damage during the reperfusion period. Mongolian gerbils were subjected to tra nsient bilateral carotid ischemia for 20 min with 2 h reperfusion. All gerbils were pretreated intraperitoneally with equivalent volumes in saline of 0.003 units per kilogram of insulin or vehicle or with 4 gra ms of glucose per kilogram. The gerbils were then scanned in a 4.7 Tes la Magnetic Resonance Imager-Spectrometer to determine levels of intra cellular pH, inorganic phosphate, adenosine triphosphate, and phosphoc reatine. In each group, intracellular pH decreased with ischemia, but most significantly in hyperglycemic animals (6.45+/-0.15), in which it had not recovered to pre ischemic levels by the end of the reperfusio n period (6.8+/-0.1 vs 7.04+/-0.1, p < 0.05). High-energy phosphates p hosphocreatine-inorganic phosphate and phosphocreatine-adenosine triph osphate showed partial recovery in all groups throughout the reperfusi on period; the recovery was not significantly altered by glucose statu s. Hyperglycemia worsened pH but not the recovery of high-energy phosp hates in animals reperfused alter 20 min of transient cerebral ischemi a. This sustained acidosis may be a primary event in transient damage in hyperglycemic animals.