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Platelet activating factor (PAF) is often used to study the effects of platelet activation. While direct myocardial electrophysiological effects of PAF have been described in superfused myocardial tissue, little is known about its actions on the whole heart. 2. The cellular electrophysiological and arrhythmogenic effects of PAF (10(-11)M, 10(-10)M and 10(-9)M) were studied during normal perfusion, global myocardial ischaemia and reperfusion in Langendorff-perfused guinea-pig hearts at 32 degrees C. 3. PAF (10(-9)M) increased the incidence of ventricular fibrillation during ischaemia and reduced action potential duration (APD) during normal perfusion and early myocardial ischaemia (10(-9)M and 10(-10)M). PAF also reduced refractory period (RP) during normal perfusion (10(-9)M) and early ischaemia (10(-9)M and 10(-10)M). PAF prevented recovery of APD (10(-9)M) and RP (10(-9)M and 10(-10)M) during reperfusion. PAF at a concentration of 10(-11)M had no electrophysiological effects. 4. PAF (10(-9)M) increased the QRS width of the electrocardiogram during late ischaemia while 10(-10)M PAF raised pacing threshold during late ischaemia. 5. Perfusion pressure was increased, and developed tension decreased by 10(-9)M PAF. 6. These results demonstrate that PAF has direct myocardial electrophysiological effects in the whole heart which occur during normal perfusion and are capable of augmenting the effects of myocardial ischaemia, but are independent of the presence of platelets.
Flores et al. (1990) studied this question.