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缺氧缺血性脑病的损伤机制:对治疗的启示

Mechanisms of injury in hypoxic-ischemic encephalopathy: implications to therapy.

作者信息

Greer David M

机构信息

Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.

出版信息

Semin Neurol. 2006 Sep;26(4):373-9. doi: 10.1055/s-2006-948317.

DOI:10.1055/s-2006-948317
PMID:16969737
Abstract

Cardiac arrest survivors commonly suffer ischemic brain injury, and understanding the mechanisms of injury is essential to providing insight for effective therapies for brain protection. Injury can occur at the time of the cardiac arrest and is dependent not only on the duration but also the degree of impaired circulation. Injury can be ongoing even after the return of spontaneous circulation, giving the clinician an additional window of opportunity to treat and protect the injured brain. This section will review the molecular basis of injury with cardiac arrest and will elucidate the different mechanisms of injury between cardiac arrest, pure respiratory arrest, and arrest secondary to toxins (e.g., carbon monoxide). The rationale for multiple postarrest therapies, such as hypothermia and induced hypertension, will also be reviewed.

摘要

心脏骤停幸存者常遭受缺血性脑损伤,了解损伤机制对于为脑保护有效疗法提供见解至关重要。损伤可发生在心脏骤停时,不仅取决于持续时间,还取决于循环受损的程度。即使在自主循环恢复后,损伤仍可能持续,这为临床医生提供了额外的治疗和保护受损大脑的机会窗口。本节将回顾心脏骤停损伤的分子基础,并阐明心脏骤停、单纯呼吸骤停和毒素(如一氧化碳)继发骤停之间不同的损伤机制。还将回顾多种骤停后治疗(如低温和诱导高血压)的基本原理。

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