The Effects of Platelet GP IIa/IIIb Receptor Blocker Abciximab on Intimal Hyperplasia After Experimental Carotid Endarterectomy

Abstract

Objective: Thrombosis and intimal hyperplasia occuring after carotid endarterectomy cause restonosis. By preventing activation of platelets and neointimal hyperplasia, carotid thrombosis and intimal hyperplasia can be impeded. In this study we applied platelet gpIIa/gpIIIb receptor blocker abciximab on rat vessel walls and examined its effect on intimal hyperplasia.

Methods: Abciximab was produced at mammiferous cell culture as fab portion of 7E3 monoclonal antibody. It inhibits platelet aggregation by binding glicoprotein IIa/IIIb receptor on platelet. It also inhibits intimal hyperplasia by binding alphaVbeta3 receptor on vitronectin of platelet, endothelial and smooth muscle cells. The carotid endarterectomy model is formed by opening the common carotid of rats and taking out the intimal layer. In group A no medication was applied to rats. In group B abciximab was applied topically. After 2 weeks intimal hyperplasia was examined histopatologically. In group A and B intimal hyperplasia ratios were measured and cytometric analysis was made. At two weeks, the rate of hyperplasia was significantly lower in group B (p<0.0007).

Conclusion: This study has shown that abciximab can reduce intimal hyperplasia occuring in rat carotid endarterectomy model.