Platelet embolic injury; the healing process

Abstract

The impaction of emboli composed mainly of platelets at the bifurcation of arterioles in the renal cortex has been shown previously to produce severe endothelial injury and lipid accumulation in arteriolar smooth muscle, followed by a marked thickening of the intima. In this study magnesium aluminum wire was inserted into the rabbit aorta as a source of emboli composed of platelet aggregates. The healing of renal arteriolar lesions produced by the emboli was examined at intervals from 3 to 21 days. The distinctive electron microscopic features of the mononuclear cells, endothelial cells, and smooth muscle cells were described. The mononuclear cells were found to remove fibrin, red cell and platelet remnants, and to produce a mucopolysaccharide matrix. Endothelium then grew into the matrix displacing the monocytes. Lipid in smooth muscle was always associated with myofilament fragmentation and mitochondrial vacuolization suggesting that the lipid accumulation is a result of injury. Plaques of concentric intimal thickening were found to consist of condensed matrix and myointimal cells. At each stage the cell types remained distinctive and there was no suggestion that monocytes are transformed to endothelial cells. These lesions serve as a model for some of the features of the encrustation concept of atherosclerosis, in that intimal thickening follows on thrombosis, in this case thromboemoblism and is associated with lipid accumulation in smooth muscle cells. The injury begins with endothelial damage and disruption. The subsequent intimal thickening resembles the vascular lesion in chronic allograft rejection and malignant nephrosclerosis and also involves the intertubular arterioles and small arteries of the kidney.