Year: 2010
Type: article
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.
Source: Signa Vitae
Language: English
Subfield: Pathology and Forensic Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2306219044