Adenosine Metabolites Are a Source of Oxygen Free Radicals in the Ischemic/Reperfused Rat Brain
Adenosine Metabolites Are a Source of Oxygen Free Radicals in the Ischemic/Reperfused Rat Brain
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腺苷代谢物是缺血/再灌注大鼠脑中氧自由基的来源
DOI：
10.1007/978-1-4615-2011-5_44
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
M. O'regan
中科院分区：
文献类型：
--
作者：
J. Phillis;M. O'regan
脑缺血再灌注损伤的病理生理特征是一系列复杂的事件，包括生化、血流动力学和电生理过程，这些过程经常导致神经元死亡。脑血流量（CBF）低于临界阈值会导致能量衰竭、组织酸中毒、细胞内Na+和Ca2+内流和K+外排的离子稳态紊乱、膜去极化和细胞毒性水肿。兴奋性氨基酸神经递质谷氨酸和天冬氨酸的大量释放，可引发细胞进一步去极化和细胞内钙积累。游离胞质Ca2+水平的增加似乎在导致不可逆神经元损伤的事件的进展中起关键作用，因为它沉淀了一系列神经毒性过程，包括自由基的产生、脂质过氧化、蛋白水解酶的激活和诱导潜在有害的原癌基因表达。
The pathophysiology of brain ischemia/ reperfusion injury is characterized by a complex sequence of events, including biochemical, hemodynamic, and electrophysiologic processes, which frequently lead to neuronal death. Decreases in cerebral blood flow (CBF) below a critical threshold result in energy failure, tissue acidosis, disturbed ion homeostasis with cellular Na+ and Ca2+ influx and K+ efflux, membrane depolarization, and cytotoxic edema. There is a massive release of the excitatory amino acid neurotransmitters, glutamate and aspartate, which can trigger further cell depolarization and intracellular calcium accumulation. The increased level of free cytosolic Ca2+ appears to play a pivotal role in the progression of events that lead to irreversible neuronal injury, in that it precipitates a series of neurotoxic processes, including free radical generation, lipid peroxidation, activation of proteolytic enzymes, and the induction of potentially injurious protooncogene expression.
缺氧/复氧诱导脑微血管中羟基自由基的形成。
影响因子：
7.4
作者：
Grammas,P;Liu,GJ;Wood,K;Floyd,RA
通讯作者：
Floyd,RA
α-苯基叔丁基硝酮 (PBN) 可减弱大鼠脑缺血再灌注损伤期间羟自由基的产生：一项 EPR 研究。
DOI：
10.3109/10715769309056513
发表时间：
1993
期刊：
Free radical research communications
影响因子：
--
作者：
Sen,S;Phillis,JW
通讯作者：
Phillis,JW