Abstract
To investigate the adaptive mechanisms following carotid artery ligation in immature rats, histologic injury and tissue levels of ATP were compared after exposure to identical episodes of hypoxia induced either 3 or 24 h postligation. Histologic injury, assessed in both 9-day- and 23-day-postnatal animals after survival for 1 week, was markedly diminished in animals exposed to hypoxia 24 h postligation compared to that in animals exposed to hypoxia 3 h postligation. In 9-day-postnatal animals, ATP levels in the cerebral cortex ipsilateral to the ligation were depleted during hypoxia to 0.39 ± 0.49 mmol/kg (mean ± SD; N = 15) in animals exposed to hypoxia 3 h postligation but were maintained at 2.04 ± 0.26 mmol/g (N = 18; p < 0.001) in animals exposed to hypoxia 24 h postligation. Thus, preservation of ATP may account for the diminution of cellular injury that results from delaying the onset of hypoxia from 3 to 24 h after carotid artery ligation in immature rats.