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M M Litrenta

Publications and source records attributed to M M Litrenta.

8 recordsLinked to original sources
PubMed1983

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. Cholesterol and saturated cholesteryl esters accumulated in cultured arterial smooth muscle cells (SMC) infected with MDV. Similar preliminary observations were made in vivo. These findings suggest that MDV-induced alteration of SMC lipid metabolism is of major importance in the pathogenesis of MDV-induced atherosclerosis. In addition, immunization with turkey herpesvirus, used commercially to prevent MDV-induced tumors in chickens, also protected against MDV-induced atherosclerosis. This animal model has introduced important new dimensions and tools in atherosclerosis research: a defined etiologic agent (MDV) that causes atherosclerosis in a defined animal of known genetic susceptibility to the etiologic agent. With these tools, important mechanisms in the pathogenesis of atherosclerosis may be established in a relatively short period of time. Further, this animal model should be considered important in other models of atherosclerosis research because herpesvirus infections are ubiquitous in these animals. Finally, because humans are widely and persistently infected with up to five herpesviruses, these studies may lead to the understanding and eventual control of human atherosclerosis.

Animals↗
PubMed1983

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. To determine whether these regions differed with respect to their glycosaminoglycan composition, the authors divided 53 rabbits into four groups. Groups IA and IB were fed a regular diet beginning 5 weeks prior to aortic deendothelialization; Groups IIA and IIB were fed the same diet supplemented with 0.5% cholesterol. The rabbits were continued on these diets following aortic deendothelialization with a balloon catheter. Those in Groups IA and IIA were sacrificed either at 2-5 weeks or 6-8 weeks following deendothelialization; proteoglycans were assessed morphometrically following staining with alcian blue. Groups IB and IIB were sacrificed at 10 weeks following injury; glycosaminoglycans were extracted from deendothelialized and reendothelialized aortas, separated by electrophoresis, and quantitated by scanning densitometry. Morphometric analysis of stained aortic sections revealed significantly increased quantities of alcianophilic material in the neointima of reendothelialized aortas as compared with deendothelialized aortas in both diet groups. Chemical analysis revealed significantly more of each glycosaminoglycan in reendothelialized aortas when compared with deendothelialized or uninjured aortas. The major glycosaminoglycans present in all regions were heparan sulfate and chondroitin sulfate; and although absolute quantities of these particular glycosaminoglycans increased in the reendothelialized region, their relative percentages remained the same for each area analyzed. Cholesterol feeding did not appear to influence glycosaminoglycan concentration and composition in reendothelialized and deendothelialized regions when compared with normal diets, but cholesterol feeding alone did increase aortic glycosaminoglycans in uninjured aortas. The results suggest that the presence of endothelium influences the quantity and type of glycosaminoglycans accumulating in the neointima, and that the differences in proteoglycans in the reendothelialized artery may account at least in part for the propensity of this area to accumulate lipid and evolve as atherosclerosis.

Animals↗
PubMed1979

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. Group I and II were inoculated intratracheally at 2 days of age with MDV. At 15 weeks, one group of virus-infected chickens (Group II) and one group of uninfected controls (Group IV) were fed a 2% cholesterol supplement for an additional 15 weeks. Group I, infected, and III, uninfected, were continued on a cholesterol-poor diet. All groups were killed at 30 weeks. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of both Groups I and II but not in those of Groups III and IV. Microscopically, arterial changes in infected animals were characterized by occlusive fibromuscular intimal thickening, which formed fibrous caps overlying areas of atheromatous change. This change closely resembled chronic atherosclerosis in humans. These results may be important to our understanding of human arteriosclerosis, since there is widespread and persistent infection of human populations with as many as five herpesviruses.

Animals↗
PubMed1978

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). In contrast, grossly visible atherosclerotic lesions were not seen in uninfected normocholesterolemic chickens (group III), nor in uninfected hypercholesterolemic chickens (group IV). Microscopically, arterial changes in the infected animals were characterized by occlusive fibromuscular intimal thickening which formed fibrous caps overlying areas of atheromatous change. This change closely resembled chronic atherosclerosis in man. These results may have important bearing on our understanding of the etiology and pathogenesis of human arteriosclerosis since there is widespread and persistent infection of human populations with up to five different herpes-viruses.

Animals↗
PubMed1978

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. aeruginosa vasculitis seldom occur. In the patient we describe, fatal Ps. aeruginosa bacteremia was first manifested by a syndrome indistinguishable from pulmonary thromboembolism with infarction.

Adult↗