RT  - Signa Vitae
ID  - 10.22514/SV51.092010.7
T1  - Protecting mitochondrial bioenergetic function
A1  - RAÚL J. GAZMURI
A1  - IYAD M. AYOUB
A1  - JEEJABAI RADHAKRISHNAN
K1  - cardiac arrest
K1  - reper-fusion injury
K1  - mitochondria
K1  - bioen-ergetic function
K1  - left ventricular myo-cardial distensibility
K1  - sodium-hydro-gen exchanger isoform-1 (NHE-1) inhibitors
K1  - erythropoietin
YR  - 2010
SP  - 32
AB  - <p>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.</p>