Kaplan J, Dimlich R V, Biros M H, Hedges J
Department of Emergency Medicine, University of Cincinnati Medical Center, OH 45267-0769.
Resuscitation. 1987 Sep;15(3):149-69. doi: 10.1016/0300-9572(87)90012-8.
Normal compensatory mechanisms protect the central nervous system (CNS) from moderate hypoxia and ischemia; however, after more severe ischemia progressive brain hypoperfusion ensues and irreversible damage occurs. Ischemic brain injury remains greatly significant clinically and elucidating the determinants of ischemic neuronal injury and death continues to challenge researchers. Although altered perfusion and decreased energy charge may contribute to the production of irreversible damage, the distribution of lesions seen after insult does not correspond with the degree of ischemic blood flow impairment, nor can neuronal energy deprivation explain the cell damage. Other factors, such as derangements in astrocyte function, calcium homeostasis, free radical metabolism, acid-base regulation and excitatory neurotransmitters also probably mediate ischemic neuronal death. Continued investigation to establish the cellular pathophysiology of cerebral ischemia can guide rational research and therapeutic strategies.
正常的代偿机制可保护中枢神经系统（CNS）免受中度缺氧和缺血的影响；然而，在更严重的缺血后，会出现进行性脑灌注不足并发生不可逆损伤。缺血性脑损伤在临床上仍然具有重大意义，阐明缺血性神经元损伤和死亡的决定因素仍然是研究人员面临的挑战。尽管灌注改变和能量电荷降低可能导致不可逆损伤的产生，但损伤后所见病变的分布与缺血性血流损害程度并不对应，神经元能量剥夺也无法解释细胞损伤。其他因素，如星形胶质细胞功能紊乱、钙稳态、自由基代谢、酸碱调节和兴奋性神经递质等，也可能介导缺血性神经元死亡。持续开展研究以确立脑缺血的细胞病理生理学，可为合理的研究和治疗策略提供指导。
