Abstract
The present study was undertaken to investigate the influence of imposed anemic hypoxia on cerebral hemodynamics and metabolism in a condition of massive ICH. Two groups of eight dogs, with a target hemoglobin concentration of 12 g/dl in nonanemic and 6 g/dl in anemic group, were included. Before the onset of the insult, anemic group had a significant reduction ( p<0.05) in cerebral arteriovenous oxygen content difference (AVDO 2), accompanied with a significant rise ( p<0.05) in flow velocity (FV) of the basilar artery and cerebral extraction fraction of oxygen (CEO 2) and a lower brain-tissue lactate clearance than did nonanemic group. Shortly after ICH, both groups displayed significant reductions ( p<0.05) in FV, CEO 2 and AVDO 2, and simultaneous rises in arteriovenous lactate concentrations. In nonanemic group, the CEO 2 and AVDO 2 gradually returned after an initial decrease, and then the arteriovenous lactate concentrations slowly decreased. In contrast, anemic group showed progressive reductions in CEO 2 and AVDO 2 associated with persistent rises in arteriovenous lactate concentrations. Consequently, anemic group exhibited significantly greater brain-tissue lactate clearances ( p<0.05), occurring at 10 min and 5 h postinjury, than did nonanemic group, although the former had relatively higher levels of CEO 2 up to 3 h postinjury. We conclude that anemic hypoxia modulates a favorable change in cerebral hemodynamics and oxygenation, while it progressively deteriorates after an initial reduction during massive ICH, thus facilitating cerebral anaerobic glycolysis in biphasic periods. These results point to a complex interaction between cerebral hemodynamics, oxygen supply and glycolysis homeostasis upon the addition of anemic hypoxia in severe stress conditions of the brain.
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