Smooth muscle cell proliferation in response to endothelial injury in coronary arteries of normal and von Willebrand's disease swine.

The proliferative response of medial smooth muscle cells to balloon-induced endothelial denudation was measured in coronary arteries of normal and von Willebrand's disease swine, a strain of swine with a genetic defect affecting platelet-vessel wall interactions. Animals were sacrificed 48 hours following endothelial injury. Incorporation of a 1-hour pulse label of 3H-thymidine was determined by measuring DNA specific activity. Autoradiography of coronary artery step segments was also performed. The ratio of DNA specific activity in ballooned vessels to that in nonballooned vessels ranged from 1.2 to 26.2. No statistically significant difference in 3H-thymidine incorporation between the two phenotypes was documented (p greater than 0.25). Similarly, DNA incorporation of 3H-thymidine as determined by autoradiography was accelerated to the same degree in ballooned vessels in both phenotypes. The results suggest that von Willebrand factor-mediated platelet activation is not essential for the release of platelet-derived growth factor or that in vivo factors other than platelet-derived growth factor play a significant role in the response of medial smooth muscle cells to acute intimal injury causing endothelial denudation.