Intracellular acidosis during and after cerebral ischemia: in vivo nuclear magnetic resonance study of hyperglycemia in cats.
In vivo 31P nuclear magnetic resonance spectroscopy was used to monitor the time course of intracellular pH in cat cerebral cortex subjected to global cerebral ischemia under control and hyperglycemic pretreatment conditions. Transient (16 minutes) global cerebral ischemia was induced in 14 cats using an inflatable cervical cuff combined with systemic arterial hypotension. Six cats were pretreated with infusion of 1.5 g/kg glucose prior to ischemia. Relative concentrations of high-energy phosphate metabolites and intracellular pH were continuously monitored before, during, and for 2 hours after cerebral reperfusion. During ischemia, intracellular pH fell to the same level and followed a similar time course in both groups. However, during initial reperfusion in the hyperglycemic group, there was a severe further decline (p less than 0.003) in intracellular pH. We suggest that the increased neurologic deficit and mortality found in hyperglycemic animals subjected to cerebral ischemia may be attributed to this transient severe tissue acidosis.
D000138:Acidosis / Q000209:etiology / Q000378:metabolism*; D000818:Animals; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism*; D002415:Cats; D002540:Cerebral Cortex / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000009:adverse effects; D006863:Hydrogen-Ion Concentration; D006943:Hyperglycemia / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D013057:Spectrum Analysis; D013997:Time Factors
D005947:Glucose