الفهرس 
Perinatal asphyxiaOnly 14 pages are availabe for public view
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Abstract
Perinatal asphyxia is an insult to the fetus or newborn due to a lack of oxygen (hypoxia) and/or a lack of perfusion (ischemia) to various organs. Hypoxic ischemic encephalopathy (HIE) describes encephalopathy as defined earlier with objective data to support a hypoxic/ischemic mechanism. Hypoxic ischemic brain injury is the most important consequence of perinatal asphyxia. Reperfusion of previously ischemic tissue may also promote the formation of excess oxygen free-radicals, which may damage cellular lipids, proteins, nucleic acids and the blood brain barrier (Aurora and Synder, 2004). Perinatal asphyxia is a major cause of immediate and postponed brain damage in the newborn and may be responsible for several delayed neurological disorders, and in this respect, early markers of brain injury would be relevant for therapeutic intervention and identification of infants at high risk (Calamandrei et al, 2004). Isoprostanes are new class of lipids, isomers of the conventional enzymatically derived prostaglandins, which are produced during peroxidation of membrane lipids by free radicals and reactive oxygen species, and are currently used as markers of many disease states and experimental conditions in which oxidative stress is a prominent feature. F2 isoprostanes are the most studied species and can provide a reliable index for the oxidant component of several diseases (Janssen, 2000; Practico et al, 2001). Number of studies have shown that isoprostanes are extremely accurate markers of lipid peroxidation in animal models of oxidative stress. Increased brain F2 isoprostane levels shortly after the asphyctic insult have shown to be predictive of delayed behavioural disturbances in animal studies (Morrow and Roberts, 1996; Cracowski et al, 2001).