Response of Cortical Oxygen Pressure and Striatal Extracellular Dopamine in the Brain of Newborn and Adult Animals to Hypoxia

The pathophysiologic mechanisms underlying hypoxic-ischemic brain damage at any age are very complex and compared to adults, newborns respond differently to similar hypoxic-ischemic insult (Duffy et al., 1982; Raichle, 1983). These is general agreement that newborns are more resistant to hypoxia/ischemia and can survive hypoxia much longer than adults of the same species (Glass et al., 1944). The greater resistance of the immature animals has been attributed to its lower cerebral metabolic rate; a greater ability to maintain energy reserves through glycolysis; lesser complexity of the synaptic connections and/or differences in the enzyme content (Duffy et al., 1972; Duffy and Vannucci, 1977; Vannucci, 1989). On the other hand, evidence had been presented that exposure to moderate hypoxia during early postnatal life may result in disruption of functional activity at selected synapses even when it does not cause histologically measurable neuronal damage (Hedner and Lundborg, 1979; 1980). Similarly, it has been proposed that exposure of immature brain to moderate hypoxia may cause permanent changes in synaptic function and have significant impact on further neuronal development (Ihle et al., 1985; Lun et al., 1986).