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1 The eects of cilostamide, a cyclic nucleotide phosphodiesterase 3 (PDE3) selective inhibitor, on vascular intimal hyperplasia were evaluated using a single-balloon injury model and a double-injury model in which the rat common carotid artery was subjected to a second injury at a site injured 14 days previously. 2 In the double-injury model, the second balloon injury caused more severe intimal hyperplasia (intima/media (IM) ratio, 1.88+0.10) than in the single-injury model (1.09+0.08). Histopathological study revealed that vascular smooth muscle cells (VSMC) were the predominant cell-type in the aected neointimal area. 3 Oral administration of cilostamide for 2 weeks after the second injury suppressed intimal hyperplasia in the double-injury model (30 mg kg 71 bid, 83% inhibition in terms of the IM ratio, P50.05; 100 mg kg 71 bid, 69% inhibition, P50.05). Similar eects were also observed in the singleinjury model with oral administration of cilostamide for 2 weeks (100 mg kg 71 bid, 36% inhibition, P50.01). 4 Cilostamide inhibited DNA synthesis of cultured VSMC stimulated by foetal calf serum or dierent kinds of growth factors, but did not aect their migration stimulated by platelet-derived growth factor (PDGF)-BB. Cilostamide signi®cantly increased the cyclic AMP concentration of VSMC dose-dependently. 5 These results indicate that cilostamide suppresses intimal hyperplasia both in the single-and double-injury models of rat, presumably by inhibiting proliferation rather than migration of VSMC. It is suggested that PDE3 inhibitors might ®nd application in preventing intimal hyperplasia following angioplasty such as percutaneous transluminal coronary angioplasty (PTCA) or stent.

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