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• W2020706964 abstract "Perinatal hypoxia-ischaemia induces a biphasic cerebral injury: the depletion in high energy phosphates during the insult returns to normal soon after resuscitation. However, some 8–15 h later a second phase of impaired energy metabolism begins, which is related to the severity of later neurodevelopmental impairment. Delayed injury differs from acute hypoxia-ischaemia because intracellular acidosis does not occur. Apoptosis may be a mechanism of delayed cellular injury. Apoptotic cells and typical DNA fragmentation have been found after perinatal hypoxia-ischaemia. In newborn piglets, fraction of apoptotic cells was directly related to the degree of high energy phosphate depletion during hypoxia-ischaemia. Apoptosis may be interrupted: in piglets, brain cooling for 12 h following resuscitation reduced the fraction of apoptotic but not necrotic cells. These results have implications for both the understanding of cerebral injury and the use of hypothermia as a neural rescue strategy in the developing brain." @default.
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• W2020706964 title "Apoptosis in perinatal hypoxic-ischaemic cerebral damage" @default.
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• W2020706964 doi "https://doi.org/10.1111/j.1365-2990.1996.tb01122.x" @default.
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