Profound acute normovolemic hemodilution has been associated with neurological functional alterations as a deficit in cognitive function and memory in experimental and clinical settings with both healthy volunteers and surgical patients submitted to cardiopulmonary bypass. Previous studies have demonstrated that ANH elicits a number of different proteins in the brain such as hypoxia inducible factor1a, vascular endothelial growth factor, neuronal and inducible nitric oxide synthase. A study with microarray analysis and ANH has also demonstrated an up-regulation of numerous genes involved in inflammatory response: angiogenesis, vascular homeostasis, and apoptosis. Among the several mechanisms that contribute to cognitive impairment, the role of hypoxia-induced neuronal Finasteride apoptosis has been studied in various scenarios. One of the key neuronal death pathways is mitochondrial, through the activation of apoptotic Bcl2 family proteins. The neuronal apoptotic pathway has been related to Bucetin hypoxic injury in several neonatal hypoxia and CPB associated hemodilution studies ; however, no study has investigated the role of these apoptotic proteins in severe acute anemia alone. This study aimed to test the hypothesis that acute normovolemic anemia with a hematocrit of 10 or 15% could induce the activation of the neuronal mitochondrial-mediated intrinsic apoptotic pathway by evaluating different cellular events involved in hypoxia-induced apoptosis and analyzing some key proteins such as Bax, Bcl-x, caspase 3 and 9, and the presence of endonucleolytic DNA fragmentation, a hallmark of apoptosis, in a porcine model of acute anemia. We evaluated the effects of acute anemia on cerebral tissue through the expression of neuronal apoptosis markers in different subcellular fractions in a model of ANH. The cortical and hippocampal regions were evaluated in this study due to their relationship to cognitive function and memory.The results showed that neither 10 nor 15% hematocrit caused hypoxiainduced apoptosis, as demonstrated by the unchanged expression of Bax, Bcl-x and caspase-3 and -9 activity and the absence of DNA fragmentation.