Transient and partial mitochondrial inhibition for the treatment of postresuscitation injury: Getting it just right-Reference-Cited by-同舟云学术

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Transient and partial mitochondrial inhibition for the treatment of postresuscitation injury: Getting it just right

Published:2006-12 Issue:Suppl Volume:34 Page:S474-S482
ISSN:0090-3493
Container-title:Critical Care Medicine
language:en
Short-container-title:Critical Care Medicine

Author:

Anderson Travis C.,Li Chang-Qing,Shao Zuo-Hui,Hoang Truc,Chan Kim Chai,Hamann Kimm J.,Becker Lance B.,Vanden Hoek Terry L.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Critical Care and Intensive Care Medicine

Reference33 articles.

1. Neutrophils are primary source of O2radicals during reperfusion after prolonged myocardial ischemia

2. Oxygen Radicals Can Induce Preconditioning in Rabbit Hearts

3. Direct measurement of free radical generation following reperfusion of ischemic myocardium.

4. Caspase-dependent cytochrome c release and cell death in chick cardiomyocytes after simulated ischemia-reperfusion

5. Oxidant injury occurs rapidly after cardiac arrest, cardiopulmonary resuscitation, and reperfusion*

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1. Organ-Specific Mitochondrial Alterations Following Ischemia–Reperfusion Injury in Post-Cardiac Arrest Syndrome: A Comprehensive Review;Life;2024-04-05

2. Research progress on the synthesis, structural modification and biological activity of stigmatellin A;Tetrahedron;2022-08

3. Inhaled Gases as Therapies for Post–Cardiac Arrest Syndrome: A Narrative Review of Recent Developments;Frontiers in Medicine;2021-01-14

4. Cardiopulmonary resuscitation ameliorates myocardial mitochondrial dysfunction in a cardiac arrest rat model;The American Journal of Emergency Medicine;2020-01

5. Cardiac Arrest;Circulation Research;2015-06-05

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