Morphologic investigation of coronary arteries subjected to hypertension by experimental supravalvular aortic stenosis in dogs.
A sustained and gradual development of hypertension in coronary arteries of 16 foxhounds was induced by afterload stress with supravalvular aortic stenosis. Dogs were perfusion fixed after 4 months and 1 year of stenosis for morphologic analysis of coronary arteries with scanning electron microscopy, transmission electron microscopy, and light microscopy. Mean prestenotic pressures and SD standard deviations in millimeters of mercury for perfusion-fixed foxhounds after 4 months were systolic 141 +/- 14, mean arterial 101 +/- 8, and diastolic 81 +/- 7, and after 1 year systolic 182 +/- 31, mean arterial 128 +/- 22, and diastolic 101 +/- 16. Scanning electron microscopy results of coronary arteries subjected to 4 months of hypertension show little change from normal coronary arteries. Only isolated cases of desquamating endothelial cells were seen directly proximal to ostia of coronary arteries. Transmission electron microscopy showed no ultrastructural changes in this banding group. In four of six foxhounds subjected to 1 year of hypertension, scanning electron microscopy observations of coronary arteries revealed one to five areas of endothelial denudation, typically oriented parallel to the longitudinal axis of the artery, a few cell diameters wide and 100 to 300 microns in length. These lesions were often seen to form narrow channels between two or more branching points, either in a continuous or in series fashion. Platelets, lymphocytes, granulocytes, and monocytes adhered to the subendothelial surface. Occasional denudations were oriented transversely to the longitudinal axis. Denudations were restricted to arteries greater than 1.2 mm in diameter. In the vicinity of denudation lesions, lymphocytes and monocytes adhered to endothelium showing alterations in cell size and shape. Transmission electron and light microscopy of this banding group showed breaks and duplication of the internal elastic lamina and smooth muscle proliferation in the intima. Focal areas of intimal inflammatory reactions, sometimes superimposed upon intimal proliferative changes, were noted in those areas exhibiting luminal cell adherence to endothelium. The results indicate that the morphologic equivalent of hypertension varies depending on the manner in which it is experimentally produced. The findings of intimal proliferation and late endothelial denudation give support to the response-to-injury hypothesis for the pathogenesis of atherosclerosis and suggest a mechanism for the role of hypertension as a risk factor.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications* / Q000503:physiopathology; D003327:Coronary Disease / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D003331:Coronary Vessels / Q000648:ultrastructure*; D004285:Dogs; D004727:Endothelium / Q000648:ultrastructure; D006439:Hemodynamics; D006973:Hypertension / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors