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Perinatal hypoxia-ischemia (HI) is considered to be a major problem of neonatology. HI may lead to hypoxic-ischemic encephalopathy (HIE). As a result o neuronal cel death and cell death and cell damage, HI can result in cerebral plasy, cognitive impairment and epilepsy . Oxidative stress is a very important factor of ischemia-induced pathogenesis of neuronal cells. Seek for effective , pharmacological therapy for hypoxia-ischemia is thus far unsuccesful. Therefore, some efforts have switched towards alternative methods, which induce brain tolerance for HI or/andwhich are associated with modification of oxygen tension. These alternative methods inculde hypobaric oxygen therapy (HBO) and mild hypobaric hypoxia postconditiong (HH) . The study showed , that both HBO and HHpostconditioning signficatantly reduced brain damage caused by HI and both methods have similar neuroprotective potential in neonatal rat HI model. One of the mechanism of neuroprotective effects of HBO and HH may be associated with reduction of oxidative stress induced by HI . Neuroproetective action of HH is probably associated with faster and more efficient neutralization of reactive oxygen species (ROS), achiieved through additional activation of antioxidant enzymes-SOD and GPx. On the other hand, neuroprotective effects of HBO may be related to the mechanisms the reduce formation of ROS in the brain after HI -it is manifested by the observed decrease in antioxidant enzymes activity , accompanied by reduction of brain damage.