Vascular innervation in atherogenesis.

Although collar-induced atherosclerosis continues to be used as an investigative tool, the underlying mechanism has not been established. Two primary mechanisms suggested are adventitial ischemia due to reduction in vasa vasorum, and perivascular denervation. We have examined the effect of injuring the common carotid artery in the pattern produced by the ends of a silastic collar, and have correlated the effect on innervation with change in intima/media ratios in normal and cholesterol-fed rabbits. The serum cholesterol of cholesterol-fed rabbits was significantly elevated by 10 days following initiation of cholesterol feeding, and further elevated at 21 days. No structural difference was detected between the uninjured carotid arteries of control and cholesterol-fed rabbits. At the site of injury in freeze injured carotid arteries there was a thickening of the intima which was increased in cholesterol-fed rabbits. The intima at the site of injury was composed of lipid-laden cells embedded in a matrix of collagen and elastin fibres. In carotid artery segments, between two sites of freeze injury, denervation was established by immunohistochemistry and electron microscopy. The denervated segments were not morphologically different from uninjured carotid arteries in either control or cholesterol-fed rabbits. While injury induced intimal thickening and foam cell development, denervation did not. It is concluded that perivascular denervation is a consequence of silastic collar application and is not involved in the induction of atherosclerosis.