Experimental intimal thickening studies using the photochemically induced thrombosis model in the guinea-pig femoral artery.

We have used the photochemically induced thrombosis model to study intimal thickening in the guinea-pig femoral artery. The femoral artery was occluded by a combination of rose bengal and green light which caused endothelial cell damage followed by formation of platelet rich thrombus at the site of endothelial damage. Thrombolysis was then achieved by administration of tissue-type plasminogen activator. Intimal thickening in the femoral arteries was histologically measured at 0, 1, 3, 6 and 9 weeks after the treatment. The neointimal areas gradually increased until 3 weeks and then remained unchanged up to 9 weeks. Cells in the neointima were identified as smooth muscle cells by immunohistochemical staining with an actin-specific antibody, HHF35. Cell proliferation in the media begun within 48 h after the thrombolysis and bromodeoxyuridine labeled cells appeared to migrate to the intima within 1 week after the thrombolysis. Administration of an angiotensin converting enzyme inhibitor, cilazapril (30 mg/kg/day, p.o.) for 3 weeks, suppressed intimal thickening and decreased the medial area in the femoral artery. These observations suggest that in this model cell proliferation and migration characteristics of pathological intimal thickening occur and this model is useful for investigating the effect of pharmacological preparations on intimal thickening.