Platelet-activating factor and granulocyte-mediated oxidative stress. Strategy for in vivo oxyradical visualization.

Platelet-activating factor (PAF) and leukotriene B4 are potent lipid mediators of endothelium-granulocyte interaction which results in granulocyte-dependent increased microvascular permeability. The specific mechanism by which PAF induces granulocyte-mediated endothelial injury has not been fully investigated. Digital imaging photonic intensified microscopy has revealed that PAF effectively induces granulocyte-mediated oxidative stress on microvascular beds. The method has made it possible to visualize luminol-dependent photonic burst released from PAF-treated microvascular beds in the rat mesentery. The photonic activities clearly corresponded to the localization of sticking granulocytes in post-capillary venules. By contrast, no significant chemilumigenic response could be detected in the leukotriene B4-induced activation of endothelium-granulocyte interaction in vivo. The present findings suggest that oxygen radicals are not prerequisites for granulocyte adhesion in the microcirculation and provide evidence for a dissociation of in vivo granulocyte function between leukotactic and oxidative activation in leukotriene B4-induced microvascular changes.