Augmented platelet recruitment in response to hyperlipidemia.

Segments of the thoracic aorta were mounted face down in a flow chamber and perfused at 24 dynes/cm² with reconstituted blood spiked with 10 000 platelets/μL that had been labeled with BCECF-am. (A) Hypercholesterolemia itself already induced a more irregular appearance of the endothelial monolayer (upper panels). The endothelial monolayer remained intact but the perfusion protocol induced slight morphologic changes, as evidenced by the rougher endothelial surface after perfusion in scanning electron microscopy, which were not different between groups (lower panels). (B,C) Hypercholesterolemia caused platelet activation as evidenced by increased translocation and firm adhesion of platelets isolated from rabbits on the diet for 3 months (3 mo) compared to control platelets on control aortas. Interestingly, the presence of lesions in the arterial tree of rabbits on the diet for a year (12 mo) did not further augment platelet translocation. Superfusion of control platelets over aortas from cholesterol-fed rabbits demonstrated an independent role for endothelial activation in response to hyperlipidemia. Endothelial and platelet activation were additive in augmenting the interaction (*P < .05; **P < .01).