Newborn piglets were subjected to 45 minutes of sustained norepinephrine-induced hypertension, and then monitored for 4, 72, or 168 hours at baseline conditions after which they were sacrificed and the anterior descending coronary artery was serially sectioned and studied by light and electron microscopy.

Changes were limited to the endothelium and subendothelial intima of the most proximal segment of the anterior descending coronary artery. As similar changes are normally present in perinatal piglets, the experimental animals were compared with sham-operated controls to determine if there was a modification of the naturally-occurring congenital lesions (Biology of the Neonate, in press).

Coronary thrombosis was not significant in either experimental (5 in 33, 15%) or control (1 in 44, 2%) animals; however, the experimental groups showed unique features. There was selective invasion of the intima by platelets and monocyte-macrophages. Isolated foamy macrophages were identified after 168 hours. At 4 hours, there was marked intimal edema, disruption of the endothelium, and fragmentation and dissolution of the internal elastic lamina. After 72 and 168 hours there was an increase in preexisting modified smooth muscle cell plaques in which there developed prominent fibroplasia and collagenization. It is proposed that rheologic trauma to the coronary wall induced by acute hypertension may be responsible for these changes and may be an initiating factor in atherogenesis.