Cyclosporine inhibits the development of medial thickening after experimental arterial injury.

Vascular proliferative lesions may occur after arterial injury and consist of inflammatory cells and proliferating smooth muscle cells. We studied the effect of cyclosporine on modulating the response to experimental arterial injury in rats. Arterial injury was created in 90 rats by rotating a 1 mm coronary dilator in the right common iliac artery. After treatment with parenteral cyclosporine 2 mg/kg/day or 5 mg/kg/day, or with saline solution, right and left iliac arteries were perfusion fixed and cross sectioned. The thickness of the tunica media was measured, and the groups were compared with a Student's t test. In the control groups the injured iliac artery had significant medial thickening when compared to the noninjured (p less than 0.05) from 1 to 42 days after injury. Injured arteries treated with cyclosporine 2 mg/kg/day for 14 days showed significantly less medial thickening when compared to controls (p less than 0.01). Cyclosporine 5 mg/kg/day for 14, 28, and 42 days showed a significant inhibition of medial thickening (p less than 0.05) for each time period. These results show that cyclosporine affects the response to experimental arterial injury by inhibiting the development of medial thickening. The most consistent effects were seen with a cyclosporine dose of 5 mg/kg/day for 2 to 6 weeks. These data also provide further evidence that immunologic mechanisms may modulate vascular proliferative lesions.