The purpose of this study was to evaluate the role of platelet-activating factor (PAF) in cardiac dysfunctions occurring in ischemic isolated rabbit heart reperfused in the presence of polymorphonuclear neutrophils (PMN) and platelets (PLT). In a first set of experiments two different PAF-receptor antagonists were used to investigate the role of endogenous PAF released in the coronary vessels of post-ischemic heart. Mechanical and electrical dysfunctions occurring during reperfusion of ischemic heart were worsened in the presence of both PMN and PLT. Co-operation between PMN and PLT was suggested by the absence of effect when reperfusion was done with PMN alone, and by the significant enhancement of the effect of PLT after addition of PMN. The activation of PMN and PLT was mediated by PAF, since it was prevented by receptor antagonists SDZ 63-675 (3 x 10(-6)M) and WEB 2170 (3 x 10(-6)M). In a second set of experiments, the infusion of PAF in non-ischemic rabbit heart perfused with PMN and PLT was used to evaluate whether PAF can induce PMN-PLT interaction and reproduce the effects of ischemia. In this condition, the infusion of synthetic PAF (1 x 10(-7)M) induced mechanical and electrical dysfunctions similar to that occurring during reperfusion. The protective effect of both PAF receptor antagonists (SDZ 63-675 and WEB 2170) and of a leukotrienes receptor antagonist (FPL 55712, 1 x 10(-6)M) suggested that PAF is the mediator that triggers the co-operation between PMN and PLT, while leukotrienes produced by these cells are the final effector of cardiac dysfunction. In conclusion, these results suggested that PAF released during reperfusion of ischemic rabbit heart may amplify mechanical and electrical dysfunctions by triggering PMN-PLT co-operation.
Platelet-activating factor (PAF) induces platelet/neutrophil co-operation during myocardial reperfusion.
ALLOATTI, Giuseppe;MONTRUCCHIO, Giuseppe;CAMUSSI, Giovanni
1992-01-01
Abstract
The purpose of this study was to evaluate the role of platelet-activating factor (PAF) in cardiac dysfunctions occurring in ischemic isolated rabbit heart reperfused in the presence of polymorphonuclear neutrophils (PMN) and platelets (PLT). In a first set of experiments two different PAF-receptor antagonists were used to investigate the role of endogenous PAF released in the coronary vessels of post-ischemic heart. Mechanical and electrical dysfunctions occurring during reperfusion of ischemic heart were worsened in the presence of both PMN and PLT. Co-operation between PMN and PLT was suggested by the absence of effect when reperfusion was done with PMN alone, and by the significant enhancement of the effect of PLT after addition of PMN. The activation of PMN and PLT was mediated by PAF, since it was prevented by receptor antagonists SDZ 63-675 (3 x 10(-6)M) and WEB 2170 (3 x 10(-6)M). In a second set of experiments, the infusion of PAF in non-ischemic rabbit heart perfused with PMN and PLT was used to evaluate whether PAF can induce PMN-PLT interaction and reproduce the effects of ischemia. In this condition, the infusion of synthetic PAF (1 x 10(-7)M) induced mechanical and electrical dysfunctions similar to that occurring during reperfusion. The protective effect of both PAF receptor antagonists (SDZ 63-675 and WEB 2170) and of a leukotrienes receptor antagonist (FPL 55712, 1 x 10(-6)M) suggested that PAF is the mediator that triggers the co-operation between PMN and PLT, while leukotrienes produced by these cells are the final effector of cardiac dysfunction. In conclusion, these results suggested that PAF released during reperfusion of ischemic rabbit heart may amplify mechanical and electrical dysfunctions by triggering PMN-PLT co-operation.
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