2000 Volume 12 Issue 2 Pages 127-137
The aim of this study was to evaluate the role of the KATP channel in the mechanism of ischemic preconditioning in whole body rat hearts using a KATP channel opener (KRN2391) and KATP channel blockade (glibenclamide) . In protocol 1, seven groups of rats were studied : a control group, animals that received Ischemic preconditioning (3 min of left coronary artery occlusion and 5 min of reperfusion, repeated twice sequentially) prior to 30 or 60 min of ischemia and following 60 min reperfusion (IP30, IP60), animals that received pharmacological preconditioning (injection of KRN2391) prior to ischemia (PP30, PP60), and animals that were not preconditioned prior to ischemia (NP30, NP60) . In protocol 2, the following four groups of rats were studied : IP30, PP30, IP30+ glibenclamide group (G-IP30) and PP 30+G (G-PP3O) group. Hemodynamics and arrhythmia were observed continuously, and infarcted size and Ca++-ATPase activity of sarcoplasmic reticulum (SR) in the Ischemic area were analyzed. There were no significant changes in hemodynamics. In protocol 1, the incidence of VT and infarcted size were significantly lower and Ca++-ATPase activity of SR was significantly higher in groups IP30, IP60 and PP30 than those of groups NP30, NP60 and PP60. In protocol 2, glibenclamide pretreatment abolished the effects of preconditioning on these parameters in both the PP and IP groups. We conclude that the KATP channel may play an important role in the rat model of preconditioning.
