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缺氧缺血性脑损伤:病理生理学、神经病理学和机制。

Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms.

机构信息

Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.

出版信息

NeuroRehabilitation. 2010;26(1):5-13. doi: 10.3233/NRE-2010-0531.

Abstract

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).

摘要

缺氧缺血性脑损伤是心脏骤停的一个众所周知的后果。单纯缺氧或组织毒性损伤,如窒息和一氧化碳中毒,可导致不同程度的损伤。损伤可能发生在损伤时,但在循环和氧合恢复后也可能持续发生损伤。损伤的性质和程度似乎取决于缺氧和缺血的严重程度、时间过程和持续时间,以及潜在的机制。本综述描述了缺氧缺血性脑损伤的病理生理学和分子基础,并区分了心脏骤停、单纯呼吸骤停和细胞毒性(如一氧化碳中毒)继发的损伤机制。

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