血小板激活因子在豚鼠正常灌注、心肌缺血及再灌注过程中的电生理和致心律失常作用。

Electrophysiological and arrhythmogenic effects of platelet activating factor during normal perfusion, myocardial ischaemia and reperfusion in the guinea-pig.

Flores N A, Sheridan D J

Academic Cardiology Unit, St. Mary's Hospital Medical School, London.

Br J Pharmacol. 1990 Nov;101(3):734-8. doi: 10.1111/j.1476-5381.1990.tb14149.x.

Abstract

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.

摘要

血小板活化因子（PAF）常用于研究血小板活化的作用。虽然PAF对灌注心肌组织的直接心肌电生理作用已有描述，但对其在整个心脏上的作用却知之甚少。2. 在32℃下，对Langendorff灌注的豚鼠心脏进行正常灌注、全心缺血和再灌注时，研究了PAF（10⁻¹¹M、10⁻¹⁰M和10⁻⁹M）的细胞电生理和致心律失常作用。3. PAF（10⁻⁹M）增加了缺血期间室颤的发生率，并缩短了正常灌注和早期心肌缺血（10⁻⁹M和10⁻¹⁰M）期间的动作电位时程（APD）。PAF还缩短了正常灌注（10⁻⁹M）和早期缺血（10⁻⁹M和10⁻¹⁰M）期间的不应期（RP）。PAF阻止了再灌注期间APD（10⁻⁹M）和RP（10⁻⁹M和10⁻¹⁰M）的恢复。浓度为10⁻¹¹M的PAF没有电生理作用。4. PAF（10⁻⁹M）增加了晚期缺血时心电图的QRS波宽度，而10⁻¹⁰M的PAF提高了晚期缺血时的起搏阈值。5. 灌注压力升高，10⁻⁹M的PAF使舒张期张力降低。6. 这些结果表明，PAF在整个心脏中具有直接的心肌电生理作用，这些作用在正常灌注期间就会出现，并且能够增强心肌缺血的影响，但与血小板的存在无关。