Complement inhibition as a proposed neuroprotective strategy following cardiac arrest

Document Type

Article

Abstract

Out-of-hospital cardiac arrest (OHCA) is a devastating disease process with neurological injury accounting for a disproportionate amount of the morbidity and mortality following return of spontaneous circulation. A dearth of effective treatment strategies exists for global cerebral ischemia-reperfusion (GCI/R) injury following successful resuscitation from OHCA. Emerging preclinical as well as recent human clinical evidence suggests that activation of the complement cascade plays a critical role in the pathogenesis of GCI/R injury following OHCA. In addition, it is well established that complement inhibition improves outcome in both global and focal models of brain ischemia. Due to the profound impact of GCI/R injury following OHCA, and the relative lack of effective neuroprotective strategies for this pathologic process, complement inhibition provides an exciting opportunity to augment existing treatments to improve patient outcomes. To this end, this paper will explore the pathophysiology of complement-mediated GCI/R injury following OHCA.

Medical Subject Headings

Animals; Brain Ischemia (pathology); Cerebral Infarction (prevention & control); Complement Inactivating Agents (metabolism); Complement System Proteins (metabolism); Disease Models, Animal; Heart Arrest (complications, therapy); Humans; Hypothermia, Induced (methods); Inflammation; Mice; Mice, Knockout; Nervous System Diseases (prevention & control); Treatment Outcome

Publication Date

1-1-2009

Publication Title

Mediators of inflammation

E-ISSN

1466-1861

Volume

2009

First Page

124384

PubMed ID

20150958

Digital Object Identifier (DOI)

10.1155/2009/124384

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