Abstract
To clucidatc thc rcpairing process and the pathological significance of a minute endothelial injury in the development of atherosclerosis, endothelial desquamation areas of 0.84 × 0.l4mm (lesion A by 1 sec. current) and of 1.68 × 0.32mm (lesion B by 5 sec.) were induced by applying a weak electric current (200μA) to the endothelium in the middle portions of the rabbit common carotid arteries. And the endothelial repairing process and the effect of hypercholesterolemia on the process were studied by scanning electron microscopy and other pathomorphologic methods The following results were obtained :
1 At 30 minutes after the injury in both animal groups fed with a normal diet and a cholesterol-rich diet, white blood cells and platelets were seen adhereing to the denuded areas, and Evans blue injected intravenously was insudated into that areas. But large thrombus was not formed
2 In both groups, the denuded areas were rapidly repaired by migration of surrounding endothelial cells at 24 hours (lesion A) or 3 days (lesion B) after injury Regenerated endothelial cells were arranged radially around the center of the injured areas
3 In the group fed with the normal diet, the injured area did not proceed to any arteriosclerotic lesions by 9 weeks after the injury In the group fed with the cholesterol diet, on the contrary, marked atherosclerotic lesions were developed in the injured regions The insudation of Evans blue into the injured areas ceased coincidentally with reendothelialization in the group fed with the normal diet, but in the group fed with the cholesterol diet, the insudation continued for 9 weeks after the injury. Accordingly it was suggested that continued increased permeability in the injured endothelium was important in the development of atherosclerosis
4 In the group fed with the cholesterol diet, circulating blood mononuclear cells having a few lipid vacuoles were seen in the subendothelium before the migration of medial smooth muscle cells into the intima 24 hours after the injury Foam cells were generally seen in the superficial layer of the thickened intima, and smooth muscle cells with a few lipid vacuoles were found in the deep layer of the intima 3 weeks after the injury Accordingly it was considered that the intimal foam cells might be derived from both circulating mononuclear cells and medial smooth muscle cells
5 Three weeks after injury in the group fed with the cholesterol died, foam cells observed on the luminal surface might be released from the thickened intima into the arterial lumen through the newly opened interendothelial junctions or the portions of new endothelial cell loss
6 Neither minute endothelial desquamation nor cholesterol feeding alone induced arteriosclerotic lesions, but the combination of them caused marked atherosclerosis in the injured areas
The present study suggested that minute endothelial desquamation which was repaired in a short period of time under a normolipidemic condition, was an important factor in development of atherosclerosis under hypercholesterolemia
