ANTI-CD31 DELAYS PLATELET ADHESION AGGREGATION AT SITES OF ENDOTHELIAL INJURY IN MOUSE CEREBRAL ARTERIOLES/

Tbe arterioles on the surface of the mouse brain (pial arterioles) wer e observed by invivo microscopy. A focus of minor endothelial damage w as produced in a single pial arteriole in each mouse by briefly, expos ing the site to a helium neon laser after an intravenous injection of Evans blue. Mice were injected 10 minutes before injury with a monoclo nal antibody (MAb) to mouse CD31, also known as platelet endothelial c ell adhesion molecule. This treatment doubled (P <.01) the time requir ed for the laser to produce a recognizable platelet aggregate. In addi tional experiments, an MAb to mouse CD61 and an MAb to mouse intercell ular adhesion molecule 1 had no effect. The data support previous obse rvations indicating that platelet adhesion/aggregation in this model i s induced by endothelial injury without exposure of basal lamina. The data are consistent with the hypothesis that the endothelial injury ex poses or activates a platelet endothelial cell adhesion molecule on th e endothelium which is blocked by the MAb directed against CD31. This may be the first demonstration of an effect of an anti-platelet endoth elial cell adhesion molecule on platelet adhesion/aggregation in vivo.