Hylton C M, Pesenson M A, Welsh F A
Division of Neurosurgery, University of Pennsylvania School of Medicine, Philadelphia, USA.
J Cereb Blood Flow Metab. 1995 Nov;15(6):1137-40. doi: 10.1038/jcbfm.1995.141.
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.
为了研究未成熟大鼠颈动脉结扎后的适应性机制,在结扎后3小时或24小时诱导相同程度的缺氧发作后,比较了组织学损伤和ATP的组织水平。在出生后9天和23天的动物存活1周后进行评估,与结扎后3小时暴露于缺氧的动物相比,结扎后24小时暴露于缺氧的动物的组织学损伤明显减轻。在出生后9天的动物中,结扎同侧大脑皮层的ATP水平在缺氧期间,结扎后3小时暴露于缺氧的动物降至0.39±0.49 mmol/kg(平均值±标准差;N = 15),而结扎后24小时暴露于缺氧的动物则维持在2.04±0.26 mmol/g(N = 18;p < 0.001)。因此,ATP的保存可能是未成熟大鼠颈动脉结扎后将缺氧发作从3小时延迟至24小时导致细胞损伤减轻的原因。