Cardioprotection from ischemia‐reperfusion injury due to Ras‐GTPase inhibition is attenuated by glibenclamide in the globally ischemic heart

• DOI: 10.1002/cbf.1353
• Publication Date: 2006-07-19T13:30:45Z
• Authors: Ibrahim Al‐Rashdan; Halit Canatan; May Al‐Maghrebi; Mariam H. M. Yousif; Shah A. Khan; Ibrahim F. Benter
• Keywords: Cardioprotection; Contractility; Preload; Ischemic Preconditioning

Abstract The present study was designed to see if acute local inhibition of Ras‐GTPase before or after ischemia (during perfusion) would produce protection against and reperfusion (I/R)‐induced cardiac dysfunction. effect glibenclamide, an inhibitor mitochondrial ATP‐sensitive potassium (mitoK ATP ) channels, on Ras‐GTPase‐mediated cardioprotection also studied. A 40 min episode global followed by a 30 in perfused rat hearts produced significantly impaired function, measured as left ventricular developed pressure ( P max end‐diastolic (LVEDP). Perfusion with FPT III I/R [FPT(pre)], enhanced recovery terms contractility. higher at the end FPT(pre)‐treated compared pre‐conditioned hearts. However, degree improvement contractility less when given only during [FPT(post)]. Combination treatment glibenclamide resulted significant reduction III‐mediated cardioprotection. These data suggest that activation signaling pathways are critical development dysfunction opening mitoK least part, contributes inhibition. Copyright © 2006 John Wiley & Sons, Ltd.