Proliferation, migration and cell renewal within the arterial wall

1. Arterial endothelial cells and adventitial fibroblasts have a higher rate of renewal than medial myocytes. As has been shown for rabbit aortic endothelial cells, the decrease with age in the cell turnover os caused by both a lengthening of the cell cycle of the proliferating cells and a reduction of the growth fraction. The arterial wall cells exhibit a heterogeneous division potential which is dependent on their position within the vessel. 2. A dilation trauma caused by a balloon catheter as well as numerous exogenous (freezing, ionizing radiation, noradrenaline application) and endogenous (hypertension, hypoxia, endotoxin shock) influences bring about more or less pronounced endothelial alterations. Probably, the secondary development of fibrocellular intimal plaques is dependent on the extent of endothelial regeneration. There is a possibility that complete re-endothelialization provides some protection against the development of plaques. 3. Proliferation kinetic characteristics of intimal cells from atherosclerotic plaques tell against the development of such plaques from one cell clone. The question whether or not proliferating intimal cells are of a monoclonal or a polyclonal origin cells for further investigations. Monocytogenic and myogenic foam cells have a relatively high proliferative activity and the ability to emigrate from atherosclerotic plaques at certain stages of their development. The "response-to-injury" hypothesis of atherosclerosis put forward by Ross (1977), which corresponds to the view held by European authors that atherosclerosis is a modified form of wound healing, is supported by the proliferation kinetic behaviour of vascular wall cells.