Pooling of blood in postischemic shock is modulated by platelet-activating factor (PAF).

In experiments on dogs, i.v. administration of platelet-activating factor (PAF) (500 ng/kg) was shown to induce hypotension which, apart from decreased myocardial contractility, was characterized by blood pooling in veins (82.6 +/- 6.8 mL/kg). This was accompanied by restriction of venous return to the heart and reduction of cardiac output (CO). During postischemic shock the cardio- and hemodynamic disturbances were similar to those induced by i.v. administration of PAF. In the postischemic shock model, preliminary blockage of PAF receptors with the PAF receptor antagonist BN 52021 (6 mg/kg, i.v.) significantly decreased the amount of blood pooled in shock from 38.7 +/- 5 to 18.3 +/- 2 mL/kg (p less than 0.01). Simultaneously, the reduction of CO and blood pressure, induced by reperfusion of the continuously ischemized tissues of a rear limb, was less significant in pretreated vs. the nontreated group. The data suggest that PAF may be involved in postischemic blood pooling and that PAF antagonists could be used to correct postischemic cardio- and hemodynamic disturbances.