Abstract
In a perfused guinea-pig heart model of myocardial isehaemia, reducing coronary flow by 95% for four successive 6 min periods caused a reproducible net loss of K + into the coronary perfusate. This was reduced in a concentration-dependent manner by ATP dependent K + channel blockers (glibenclamide and glipizide) and calcium channel blockers (verapamil and nifedipie). Other K + channel blockers (UK-66,914, 4-aminopyridine, R56865 and phentolamine) and β 1-adrenoceptor and β 2-adrenoceptor antagonists (betaxolol and ICI 118551) did not reduce this loss significantly. A single 30 min low-flow period reliably induced K + release and ventricular fibrillation in control hearts. Glibenclamide, glipizide and phentolamine suppressed ventricular fibrillation but not ischaemic K + loss in this model. R56865 and 4-aminopyridine and coadministration of betaxolol and ICI 18551 yielded similar results while UK-66,914 suppressed neither. In our model, modulation of ischaemic K + loss and suppression of ventricular fibrillation were not closely associated and appeared to occur via separate mechanisms.
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