Hyperglycemic versus normoglycemic stroke: topography of brain metabolites, intracellular pH, and infarct size.

摘要: Hyperglycemia aggravates brain pathologic outcome following middle cerebral artery (MCA) occlusion in cats. We presently determined if hyperglycemia during leads to high lactic acid accumulations the ischemic MCA territory. measured metabolite concentrations 14 territory sites at 0.5 and 4 h hyper- (20 mM) normoglycemic (5 cats correlated these results with previous findings. Hyper- versus normoglycemia resulted significantly higher lactate more numerous loci lactates greater than 17 mumol/g. At of occlusion, ATP levels were lower cats, while h, was similarly reduced (40%) both glycemia groups. PCr hyperglycemics secondary a tissue acidosis. Carbohydrate substrates markedly depleted normoglycemics, likely limiting accumulation (34.3% only 5.0% glucose less mumol/g). Although elevated hyperglycemic territories, clip release yields poorer outcome. Correspondingly, intracellular pH, calculated from creatine kinase equilibrium, depressed demonstrating time-dependent dissociation between hydrogen ion accumulations. The present findings show that (a) increases magnitude topographic extent marked acidosis, (b) infarct size correlates closely acidosis concentrations, (c) correlate poorly size, (d) limits focal ischemia because is depleted, (e) early ischemia, buffering or antiport mechanisms may prevent activity.