Regeneration in Large Blood Vessels Following Mild Mechanical Trauma

Abstract

Earlier investigations by Gottlob and Zinnerl showed distinct differences in the morphologically characterized changes between hard and mild mechanical trauma on blood vessels with light microscopy of silver-stained surface preparations. Whereas hard mechanical trauma, induced by ligation of the vessel wall with thick silk thread, produced complete endothelial cell destruction at the ligated area and eventual overgrowth by regenerating endothelial cells, mild mechanical trauma induced by compressing the vessel wall with a clamp covered by rubber tubing was characterized by early focal endothelial injury, eventual formation of multinucleated endothelial cells and endothelial phagocytosis of blood cell degradation products. Although hard mechanical trauma has been used by a number of investigators as a model for studies on thrombosis and endothelial regeneration, it is felt that mild mechanical trauma mimics more closely pathophysiologic phenomena in human circulation, such as inflammation, aging and surgical injury. Furthermore, recent investigations by Friedman and Byers2 have indicated that mechanical injury to the intimal lining of the arterial wall enhances atherosclerosis in cholesterol-fed rabbits. It would be of interest to see if any of the morphologic changes characteristic of very early atherosclerosis could be observed at periods following mild mechanical trauma even without inducing hyperlipemia. An investigation with the electron microscope was undertaken to study morphologic alterations in the wall of the rabbit abdominal aorta and inferior vena cava at periods ranging from one to seven days following application of mild mechanical trauma. It was felt that under the high resolution of the electron microscope, one would obtain additional information to the light microscopic studies on mild mechanical trauma previously performed. A rubber-coated bulldog clamp was applied concurrently to the rabbit abdominal aorta and inferior vena cava at the level of the renal bifurcation for 10 sec. At periods of one, two, three, five and seven days after inducing injury, the blood vessels were fixed with glutaraldehyde by an in situ perfusion technique, then excised and carried through the standard electron microscopy procedure.In contrast to what one would have expected, no progression of changes in the ultrastructural morphology of the blood vessels could be found between one and seven days after trauma. The following changes were observed at all times investigated both in the aorta and vena cava.