It is interesting that increased levels of pro-apoptotic proteins in relation to anti-apoptotic proteins and fragmentation changes as a surrogate for apoptosis were only demonstrated by the hypoxia group, while the hematocrit 10 and 15% groups did not demonstrate any change. Alosetron during hemodilution and anemia, increased blood flow is preferentially directed to cerebral circulation to guarantee brain oxygen transport. The cerebral blood flow increases in proportion to the degree of anemia, as demonstrated in clinical and laboratory studies. This, along with other compensatory mechanisms, guarantees adequate cerebral oxygen tension during acute hemodilution until oxygen consumption becomes supply-dependent. Although cerebral blood flow was not measured in our study, we can infer its preservation as oxygen delivery was maintained throughout the study. An increase in the oxygen extraction rate was observed in the hemodiluted groups, with maintenance of VO2I despite a significant decrease in DO2I that most likely contributed to oxygen supply adequacy to neuronal cells at this level of anemia. This mechanism can explain why hematocrits of 10 or 15% did not increase the Bax expression in the total frontal cortex, neuronal nuclei or Bavachin mitochondrial fractions compared to the Sham group. Low levels of hematocrit during hemodilution has been accepted during the perioperative period because of its short duration and low oxygen consumption during anesthesia. This corroborates our results, as hemodilution lasted 1.5 hours and the 10% hematocrit was safe for cerebral tissue. We do not know if an increased observation time would provoke a different result. The present investigation intended to mimic a situation likely to occur in certain surgical situations where a 10�C15% hematocrit level could be acceptable for a short period of time due to the transfusion trigger guidelines strongly recommending transfusions with a hematocrit level below 21%.The augmented pro-apoptotic/anti-apoptotic protein ratio in the mitochondrial fraction can change mitochondrial membrane permeability and the apoptotic protease activating factor-1-mediated activation of procaspase 9 in caspase 9 that subsequently activates procaspase 3 in caspase 3, which is responsible for cellular death.