The ultrastructure of the stages of atheroembolic occlusion of renal arteries.

Atheromatous material enucleated from human atheromas was injected into the left renal arteries of 25 male rabbits. The kidneys were removed at varying periods after injection and the impacted atheromatous emboli with their surrounding tissue processed for electron microscopy. The ultrastructural changes in atheroembolism were followed by killing the animals at 30 minutes, 1, 2, 6 and 48 hours and 3, 4, 6, 7, 15 days and one month. The ultrastructural changes could be divided into 3 periods. The early period (30 min-2 days) was characterized by the induction of an occlusive thrombus in which was incorporated cholesterol crystals, myelin figures, debris, platelet aggregates and fibrin. The intermediate period (2-4 days) was characterized by partial, temporary resolution of the occlusive thrombus, often with the reforming of portion of the lumen by the covering of the crystals by the endothelial cells, which in these circumstances appear particularly labile as to their anchorage sites. Cholesterol crystals were coated with an electron dense layer at this stage and there were numbers of adherent platelets on their surfaces. The late period (5 days-1 month) was characterized by extensive fibrosis around the cholesterol crystals and by cells closely allied to the smooth muscle cells which had undergone fibroblastic change. The passages between crystals were now lined completely by endothelial cells in a new capillary-like form. There appeared to be migration of smooth muscle cells into the original lumen to surround cholesterol crystals. The cholesterol crystals themselves frequently impacted in a diameter of the elastic laminae encircling the vessel. The elastic laminae did not undergo extensive change and remained to delimit the original lumen of the vessel, in some instances until the late stage.