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European Heart Journal 1994 15(Supplement C):89-94; doi:10.1093/eurheartj/15.suppl_C.89
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Cardioprotective Actions of Potassium Channel Openers

J. A. Auchampach, M. Maruyama and G. J. Gross

Department of Pharmacology and Toxicology, Medical College of Wisconsin Milwaukee, Wisconsin 53226 U.S.A.

Correspondence. Professor Garrett J. Gross. PhD. Department of Pharmacology and Toxicology, Medical College of Wisconsin. 8701 Watertown Plank Road, Milwaukee. Wisconsin 53226 U.S.A.

The potential cardioprotective effect of two pure potassium channel openers, bimakalim (EMD 52692) and aprikalim (RP 52891), on myocardial ischaemia/reperfusion injury was investigated in barbital-anaesthetized dogs. In a model of reversible ischaemia/reperfusion injury, administration of bimakalim as an intravenous bolus prior to ischaemia or administration of a non-hypotensive dose of aprikalim as a constant intravenous infusion resulted in a reduction in reperfusion contractile dysfunction (myocardial ‘stunning’) produced by a single 15-min coronary artery occlusion. Administration of aprikalim only during the reperfusion period had no beneficial effect. Similarly, in a model of irreversible ischaemia/reperfusion injury (90 min of coronary artery occlusion followed by 5 h of reperfusion), intravenous infusion of bimakalim at a dose which reduced aortic blood pressure approximately 15–20 mm Hg or infusion of aprikalim at a non-hypotensive dose throughout the entire experiment produced a significant reduction in myocardial infarct size. A protective effect of bimakalim was not observed when it was administered during ihe reperfusion period only. In both the stunned myocardium model as well as the infarcted myocardium model, the beneficial effects of the potasslum channel openers could not be attributed to differences in the traditional determinants of the extent of ischaemia/reperfusion injury; area at risk size, oxygen consumption, or collateral blood flow. Furthermore, the anti-ischaemic actions of the potassium channel openers were blocked by pre-treatment with the ATPdependent potassium (KATP) channel antagonist, glibenclamide. These results indicate that bimakalim and aprikalim are protective in two experimenta1 models of ischaemia/reperfusion injury and that the mechanism of action of these agents appears to be the result of a direct cardioprotective effect secondary to myocardtal KATP channel activation.

Key Words: Potassium channel openers • myocardial ischaemia • ATP-dependent potassium channels • bimakalim • aprikalim


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