Abstract
Endothelial cell injury is considered to be the primary event in atherogenesis. We investigated the effects of materials released from white thrombi and hypercholesterolemia on endothelial cells and the vascular wall of rabbit aorta 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 to induce vessel wall injury and thrombotic events. Then the non-injuried segments from the descending thoracic and abdominal aortas was morphologically examined. 3H-Thymidine uptake into endothelial cells and smooth muscle cells are also examined.These aortas of experimental rabbits showed endothelial damage and ensuing endothelial replication. Modified smooth muscle cells were noted in the subendothelial layer, and in the 24-week experimental group, cellular intimal thickening was also induced. 3H-Thymidine uptake into the intima and media significantly increased in the experimental group. Administration of ASA, TXA2 synthetase inhibitor (CV4151), and heparin partly reduced the endothelial damage and smooth muscle cell proliferation. Hypercholesterolemia also could cause endothelial damage, and a combination of materials released from white thrombi and hypercholesterolemia showed an additive effect on the aortic wall in vivo.
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