Hypoxic-ischemic brain injury: Pathophysiology, neuropathology and mechanisms

被引:267
作者
Busl, Katharina M. [1 ]
Greer, David M. [1 ]
机构
[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02114 USA
关键词
TRANSIENT FOREBRAIN ISCHEMIA; GLOBAL CEREBRAL-ISCHEMIA; RAT HIPPOCAMPAL SLICE; NITRIC-OXIDE SYNTHASE; CARDIAC-ARREST; PROTEIN-SYNTHESIS; CIRCULATORY ARREST; GERBIL HIPPOCAMPUS; CELL-DEATH; CARDIOCIRCULATORY ARREST;
D O I
10.3233/NRE-2010-0531
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Hypoxic-ischemic brain injury is a well known consequence of cardiac arrest. Variable injuries can occur with purely hypoxic or histotoxic insults such as asphyxiation and carbon monoxide poisoning. The injury may happen at the time of the insult, but there may also be continued damage after circulation and oxygenation are reestablished. The nature and extent of the damage appears to depend on the severity, time course and duration of the oxygen deprivation and lack of blood supply, as well as on the underlying mechanism. This review describes the pathophysiological and molecular basis of hypoxic ischemic brain injury, and differentiates between the mechanisms of injury by cardiac arrest, pure respiratory arrest, and arrest secondary to cytotoxicity (e.g. carbon monoxide poisoning).
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页码:5 / 13
页数:9
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