It is widely held that the disturbance in the integrity of the arterial endothelium may lead to the development of arteriosclerosis and many factors have been postulated to cause the endothelial injury, such as hemodynamic stress, anoxia, platelet-releasing materials, and so on. However, whether any of these is important for endothelial injury is unclear. We studied whether the released products from activated platelets and/or thrombi could cause endothelial damage and proliferation of smooth muscle cells in large vessels in vivo.Polyethylene tubing was inserted into the ascending aorta of rabbits via the common carotid artery and placed for one, 4, and 24 weeks continuously to induce vessel wall injury and thrombotic events. Then the direct non-injured segments from the descending thoracic and abdominal aorta was morphologically examined, and 3H-thymidine incorporation into the arterial wall was also examined. The descending aortas of experimental rabbits showed endothelial damage and increased mitoses of endothelial cells. Modified smooth muscle cells were noted in the subendothelial layer, and 3H-thymidine incorporation into the intima and media significantly increased in the experimental group at one week(Fig.). At 24 weeks, the intimal thickening with smooth muscle cell proliferation was also found.This experiment indicates that materials released from the activated platelets and/or thrombi into the circulation can cause endothelial damage and smooth muscle cell proliferation and intimal thickening at downstream and remote aortic segments.
Blockade of Vascular Smooth Muscle Cell Proliferation and Intimal Thickening After Balloon Injury by the Sulfated Oligosaccharide PI-88
