Apoptosis in perinatal hypoxic-ischaemic cerebral damage |
| |
Authors: | A. D. Edwards H. Mehmet |
| |
Affiliation: | Weston Laboratory, Department of Paediatrics and Neonatal Medicine, Royal Postgraduate Medical School. Hammersmith Hospital, London. UK |
| |
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. |
| |
Keywords: | apoptosis perinatal hypoxia-ischaemia |
|
|