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Review article

Protecting mitochondrial bioenergetic function

Raúl J. Gazmuri orcid id orcid.org/0000-0002-3848-7227 ; Medical Service (111F), North Chicago VA Medical Center, 3001 Green Bay Road, North Chicago, Illinois, 60064, USA. Resuscitation Institute at Rosalind Franklin University, Section of Critical Care Medicine Medical Service at the James A. Lovell Federal
Iyad M. Ayoub ; Medical Service (111F), North Chicago VA Medical Center, 3001 Green Bay Road, North Chicago, Illinois, 60064, USA. Resuscitation Institute at Rosalind Franklin University, Section of Critical Care Medicine Medical Service at the James A. Lovell Federal H
Jeejabai Radhakrishnan ; Medical Service (111F), North Chicago VA Medical Center, 3001 Green Bay Road, North Chicago, Illinois, 60064, USA. Resuscitation Institute at Rosalind Franklin University, Section of Critical Care Medicine Medical Service at the James A. Lovell Federal H


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Abstract

Reversal of cardiac arrest requires reestablishment of aerobic metabolism by reperfusion with oxygenated blood of tissues
that have been ischemic for variables periods of time. However, reperfusion concomitantly activates a myriad of pathogenic
mechanisms causing what is known as “reperfusion injury.” At the center of reperfusion injury are mitochondria, playing a
critical role as effectors and targets of injury. Mitochondrial injury compromises oxidative phosphorylation and the ability to
regenerate Adenosine-5'-triphosphate (ATP); i.e., bioenergetic function. Thus targeting mitochondria to protect bioenergetic
function may represent a novel concept in resuscitation with the potential for altering clinical practice. We have identified
sodium-hydrogen exchanger isoform-1 (NHE)-1 inhibition and erythropoietin as attractive candidate drugs for this purpose
and demonstrated corresponding functional and clinical benefits. Further work on the subject may pave the way for further
scientific discover focused on greater understating of underlying cell mechanisms, identification of additional and perhaps
more potent strategies, and develop means for effective drug delivery.

Keywords

cardiac arrest; reperfusion injury; mitochondria; bioenergetic function; left ventricular myocardial distensibility; sodium-hydrogen exchanger isoform-1 (NHE-1) inhibitors; erythropoieti

Hrčak ID:

59434

URI

https://hrcak.srce.hr/59434

Publication date:

1.9.2010.

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