Ultrastructural alterations in nutritional cardiomyopathy of selenium-vitamin E deficient swine. II. Vascular lesions

Selenium-vitamin E deficiency was produced in weanling swine by feeding a semisynthetic basal diet for 13 to 59 days. Pigs were killed sequentially for morphologic studies of the cardiac lesions. In hearts with vascular damage, gross hemorrhages were scattered in the myocardium and serosal surfaces. Light and electron microscopic study revealed myocardial arteriolar damage characterized by segmental fibrinoid accumulation in vessel walls and by scattered fibrin thrombi. Ultrastructural study disclosed extensive subendothelial and inner wall accumulations of dense granular deposits of serum proteins and masses of fibrin in arterioles in which dense deposits of fibrinoid were identified by light microscopy. Endothelial cells of these arterioles were loosely attached to each other. In arterioles with fibrin thrombi, the endothelium was disrupted. In mildly injured arterioles, increased endothelial permeability resulted in insudation of blood proteins into the vessel wall to produce accumulation of fibrinoid. In severely injured vessels, endothelial integrity was destroyed, smooth muscle cells were necrotic and thrombosis had developed. Initiation of these arteriolar lesions was apparently the result of lipoperoxidative damage to endothelial cell membranes that lacked protection by selenium-vitamin E.