EFFECTS OF PLATELET-ACTIVATING-FACTOR ON LEFT-VENTRICULAR PERFORMANCEIN DOGS

To elucidate the mechanism by which platelet-activating factor (PAF) d ecreases cardiac output (GO), its effects on left ventricular (LV) per formance were studied using a LV pressure-volume model in 9 anesthetiz ed dogs. LV volume was measured with a conductance catheter and LV pre ssure with a manometer-tipped catheter. The slopes of the end-systolic pressure-volume (E(es)), stroke work-end-diastolic volume (M(w)), and arterial end-systolic pressure-stroke volume relations (E(a)), and of end-diastolic pressure-volume relations (EDPVRs), were obtained to ev aluate changes in LV performance. The time constant of isovolumetric r elaxation (T) was computed by a logarithmic and a derivative method. A fter intravenous administration of PAF (1 mu g/kg), LV end-diastolic v olume and pressure, end-systolic pressure, maximum dP/dt and CO decrea sed. E(es) and M(w) decreased significantly, minimum dP/dt decreased, and T increased, The arterial end-systolic pressure-stroke volume rela tion shifted leftward with an increase in the slope (E(a)), whereas ED PVRs were shifted to the left and superimposed on their potential pass ive diastolic properties. These findings indicate that PAF decreases C O by reducing preload and contractility and by increasing arterial loa d. However, despite a prolongation of relaxation, PAF may not affect p assive diastolic chamber stiffness.