Cerebral energy metabolism during hypoxia-ischemia and early recovery in immature rats.
Cerebral energy metabolism during hypoxia-ischemia and early recovery in immature rats.
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未成熟大鼠缺氧缺血期间的脑能量代谢和早期恢复。
DOI：
10.1152/ajpheart.1992.262.3.h672
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Vannucci,RC
中科院分区：
文献类型：
--
作者：
Yager,JY;Brucklacher,RM;Vannucci,RC
细胞能量稳态的持续改变可能会导致围产期脑缺氧缺血引起的脑损伤。因此，分析了未成熟大鼠缺氧缺血和早期恢复期间高能磷酸盐储备的扰动的存在和程度。出生后 7 天的大鼠接受单侧颈总动脉结扎，并在 37℃ 下用 8% 氧气缺氧 3 小时，这种损伤会对 92% 的动物与颈总动脉结扎同侧的大脑半球造成损伤（选择性神经元坏死或梗死）。在缺氧缺血期间以及恢复后 10、30 和 60 分钟以及 4 和 24 小时将大鼠幼崽快速冷冻在液氮中，以进行磷酸肌酸 (PCr)、肌酸、ATP、ADP 和 AMP 的酶促荧光分析。在缺氧缺血期间，PCr、ATP 和总腺嘌呤核苷酸分别比对照减少 87%、72% 和 50%。在恢复过程中，PCr、ATP 和总腺嘌呤核苷酸表现出快速（10 分钟内）但不完全且异质的恢复，并持续至少 24 小时。 PCr 平均值保持在对照的 55% 至 85% 之间，而 ATP 值保持在对照的 57% 至 67% 之间。恢复10分钟时个体ATP值与组织含水量呈负相关，表明能量恢复失败与脑水肿程度密切相关，而脑水肿程度是脑损伤的反映。因此，高能磷酸盐储备在缺氧缺血恢复过程中表现出持续的变化。能量恢复的动物间差异可能反映了围产期脑缺氧缺血模型中所见的脑损伤范围。
Persistent alterations in cellular energy homeostasis may contribute to the brain damage that evolves from perinatal cerebral hypoxia-ischemia. Accordingly, the presence and extent of perturbations in high-energy phosphate reserves were analyzed during hypoxia-ischemia and the early recovery period in the immature rat. Seven-day postnatal rats were subjected to unilateral common carotid artery ligation and hypoxia with 8% oxygen at 37 degrees C for 3 h, an insult that produces damage (selective neuronal necrosis or infarction) of the cerebral hemisphere ipsilateral to the common carotid artery ligation in 92% of animals. Rat pups were quick frozen in liquid nitrogen during hypoxia-ischemia and at 10, 30, and 60 min and 4 and 24 h of recovery for enzymatic, fluorometric analysis of phosphocreatine (PCr), creatine, ATP, ADP, and AMP. During hypoxia-ischemia, PCr, ATP, and total adenine nucleotides were decreased by 87, 72, and 50% of control, respectively. During recovery, PCr, ATP, and total adenine nucleotides exhibited a rapid (within 10 min) although incomplete and heterogeneous recovery that persisted for at least 24 h. Mean values for PCr remained between 55 and 85% of control, whereas ATP values remained between 57 and 67% of control. Individual ATP values were inversely related to tissue water content at 10 min of recovery, indicating a close correlation between failure of energy restoration and the extent of cerebral edema as a reflection of brain damage. Thus high-energy phosphate reserves display lingering alterations during recovery from hypoxia-ischemia. The interanimal variability in energy restoration presumably reflects the spectrum of brain damage seen in this model of perinatal cerebral hypoxia-ischemia.