Effects of platelet-activating factor on left ventricular performance in dogs

To elucidate the mechanism by which platelet-activating factor (PAF) decreases cardiac output (CO), its effects on left ventricular (LV) performance were studied using a LV pressure-volume model in 9 anesthetized dogs. LV volume was measured with a conductance catheter and LV pressure with a manometer-tipped catheter. The slopes of the end-systolic pressure-volume (Ees), stroke work-end-diastolic volume (Mw), and arterial end-systolic pressure-stroke volume relations (Ea), and of end-diastolic pressure-volume relations (EDPVRs), were obtained to evaluate changes in LV performance. The time constant of isovolumetric relaxation (T) was computed by a logarithmic and a derivative method. After intravenous administration of PAF (1 microgram/kg), LV end-diastolic volume and pressure, end-systolic pressure, maximum dP/dt and CO decreased. Ees and Mw decreased significantly, minimum dP/dt decreased, and T increased. The arterial end-systolic pressure-stroke volume relation shifted leftward with an increase in the slope (Ea), whereas EDPVRs were shifted to the left and superimposed on their potential passive diastolic properties. These findings indicate the PAF decreases CO by reducing preload and contractility and by increasing arterial load. However, despite a prolongation of relaxation, PAF may not affect passive diastolic chamber stiffness.