Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest
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 circu...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2009-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2009/124384 |
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| _version_ | 1832550473286025216 |
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| author | Brad E. Zacharia Zachary L. Hickman Bartosz T. Grobelny Peter A. DeRosa Andrew F. Ducruet E. Sander Connolly |
| author_facet | Brad E. Zacharia Zachary L. Hickman Bartosz T. Grobelny Peter A. DeRosa Andrew F. Ducruet E. Sander Connolly |
| author_sort | Brad E. Zacharia |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-2b29f388e5e340919fc2b45ac2b414f4 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2009-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-2b29f388e5e340919fc2b45ac2b414f42025-02-03T06:06:36ZengWileyMediators of Inflammation0962-93511466-18612009-01-01200910.1155/2009/124384124384Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac ArrestBrad E. Zacharia0Zachary L. Hickman1Bartosz T. Grobelny2Peter A. DeRosa3Andrew F. Ducruet4E. Sander Connolly5Department of Neurological Surgery, Columbia University, 710 W. 168th Street, New York, NY 10032, USADepartment of Neurological Surgery, Columbia University, 710 W. 168th Street, New York, NY 10032, USADepartment of Neurological Surgery, Columbia University, 710 W. 168th Street, New York, NY 10032, USADepartment of Neurological Surgery, Columbia University, 710 W. 168th Street, New York, NY 10032, USADepartment of Neurological Surgery, Columbia University, 710 W. 168th Street, New York, NY 10032, USADepartment of Neurological Surgery, Columbia University, 710 W. 168th Street, New York, NY 10032, USAOut-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.http://dx.doi.org/10.1155/2009/124384 |
| spellingShingle | Brad E. Zacharia Zachary L. Hickman Bartosz T. Grobelny Peter A. DeRosa Andrew F. Ducruet E. Sander Connolly Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest Mediators of Inflammation |
| title | Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest |
| title_full | Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest |
| title_fullStr | Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest |
| title_full_unstemmed | Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest |
| title_short | Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest |
| title_sort | complement inhibition as a proposed neuroprotective strategy following cardiac arrest |
| url | http://dx.doi.org/10.1155/2009/124384 |
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