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Am J Physiol Heart Circ Physiol 279: H2350-H2359, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 5, H2350-H2359, November 2000

Differential role of KATP channels in late preconditioning against myocardial stunning and infarction in rabbits

Hitoshi Takano, Xian-Liang Tang, and Roberto Bolli

Experimental Research Laboratory, Division of Cardiology, University of Louisville, and the Jewish Hospital Heart and Lung Institute, Louisville, Kentucky 40292

The role of ATP-sensitive potassium (KATP) channels in the late phase of ischemic preconditioning (PC) remains unclear. Furthermore, it is unknown whether KATP channels serve as end effectors both for late PC against infarction and against stunning. Thus, in phase I of this study, conscious rabbits underwent a 30-min coronary occlusion (O) followed by 72 h of reperfusion (R) with or without ischemic PC (6 4-min O/4-min R cycles) 24 h earlier. Late PC reduced infarct size ~46% versus controls. The KATP channel blocker 5-hydroxydecanoic acid (5-HD), given 5 min before the 30-min O, abrogated the infarct-sparing effect of late PC but did not alter infarct size in non-PC rabbits. In phase II, rabbits underwent six 4-min O/4-min R cycles for 3 consecutive days (days 1, 2, and 3). In controls, the total deficit of systolic wall thickening (WTh) after the sixth reperfusion was reduced by 46% on day 2 and 54% on day 3 compared with day 1, indicating a late PC effect against myocardial stunning. Neither 5-HD nor glibenclamide, given on day 2, abrogated late PC. The KATP channel opener diazoxide, given on day 1, attenuated stunning, and this effect was completely blocked by 5-HD. Thus the same dose of 5-HD that blocked the antistunning effect of diazoxide failed to block the antistunning effects of late PC. Furthermore, when diazoxide was administered in PC rabbits on day 2, myocardial stunning was further attenuated, indicating that diazoxide and late PC have additive anti-stunning effects. We conclude that KATP channels play an essential role in late PC against infarction but not in late PC against stunning, revealing an important pathogenetic difference between these two forms of cardioprotection.

myocardial ischemia; myocardial reperfusion; 5-hydroxyldecanoidic acid; glibenclamide; diazoxide


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