Marked anemic hypoxia deteriorates cerebral hemodynamics and brain metabolism during massive intracerebral hemorrhage.

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 (AVDO2), accompanied with a significant rise (p<0.05) in flow velocity (FV) of the basilar artery and cerebral extraction fraction of oxygen (CEO2) and a lower brain-tissue lactate clearance than did nonanemic group. Shortly after ICH, both groups displayed significant reductions (p<0.05) in FV, CEO2 and AVDO2, and simultaneous rises in arteriovenous lactate concentrations. In nonanemic group, the CEO2 and AVDO2 gradually returned after an initial decrease, and then the arteriovenous lactate concentrations slowly decreased. In contrast, anemic group showed progressive reductions in CEO2 and AVDO2 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 CEO2 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.