Effect of endothelium on glycosaminoglycan accumulation in injured rabbit aorta.

Previous studies have indicated that reendothelialized regions of injured rabbit aortas are more susceptible to diet-induced atherosclerosis than persistently deendothelialized regions or uninjured aortas. However, the mechanism responsible for this selective lipid deposition is not understood. One possibility is that these regions differ with respect to the quantity and type of glycosaminoglycan-containing proteoglycans which are known to interact with lipoproteins.

Herpesvirus-induced atherosclerosis in chickens.

Repeated experiments have established that infection with Marek's disease herpesvirus (MDV) leads to atherosclerosis in specific pathogen free (SPF) normocholesterolemic chickens. Neither normocholesterolemic nor hypercholesterolemic uninfected SPF chickens develop this disease. The MDV-induced arterial disease is remarkably similar to chronic human atherosclerosis.

Atheroarteriosclerosis induced by infection with a herpesvirus.

Atheroarteriosclerosis closely resembling that in humans was induced in normocholesterolemic and hypercholesterolemic chickens by infection with Marek's disease herpesvirus (MDV). Four comparably sized groups of chickens were used. Each group was initially fed a diet relatively poor in cholesterol.

Bacterial invasion of pulmonary vessels. Pseudomonas bacteremia mimicking pulmonary thromboembolism with infarction.

Pseudomonas aeruginosa displays a curious propensity for invading blood vessels and causing vessel wall necrosis. This bacteremia-related "vasculitis" is often associated with hemorrhagic necrosis and infarction of surrounding organ parenchyma. With the exception of skin lesions, however, clinical manifestations of Ps.

Virus-induced atherosclerosis.

Of four groups of chickens, two (groups I and II) were infected with MDV and two were not (groups III and IV). Groups I and III were fed diets low in lipid, and groups II and IV were fed cholesterol-supplemented diets. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of infected normocholesterolemic and hypercholesterolemic chickens (groups I and II).