Intracellular sodium hydrogen exchange inhibition and clinical myocardial protection.
Although the mechanisms underlying ischemia/reperfusion injury remain elusive, evidence supports the etiologic role of intracellular calcium overload and oxidative stress induced by reactive oxygen species. Activation of the sodium hydrogen exchanger (NHE) is associated with intracellular calcium accumulation. Inhibition of the NHE-1 isoform may attenuate the consequences of this injury. Although there is strong preclinical and early clinical evidence that NHE inhibitors may be cardioprotective, definitive proof of this concept in humans awaits the results of ongoing clinical trials.
Mentzer
Robert M
RM
Department of Surgery, University of Kentucky, Lexington, Kentucky 40536, USA. mentzer@pop.uky.edu
Lasley
Robert D
RD
Jessel
Andreas
A
Karmazyn
Morris
M
D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001026:Coronary Artery Bypass; D003402:Creatine Kinase / Q000097:blood; D004232:Diuretics / Q000494:pharmacology; D006146:Guanidines / Q000494:pharmacology; D006801:Humans; D007150:Immunohistochemistry; D019157:Ischemic Preconditioning, Myocardial; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors* / Q000378:metabolism / Q000502:physiology; D013450:Sulfones / Q000494:pharmacology
D004232:Diuretics; D006146:Guanidines; D017923:Sodium-Hydrogen Exchangers; D013450:Sulfones; C069139:growth factor-activatable Na-H exchanger NHE-1; D000584:Amiloride; C093373:cariporide; D003402:Creatine Kinase