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.
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Hylton et al. (1995) studied this question.
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