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Results for “experimental evolution”

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At least 55 records · Page 3Linked to original sources
PubMed1976

Effect of reticuloendothelial stimulators on the tissue changes and evolution of experimental atheroma in rabbits.

Administration of histamine phosphate or glycerol trioleate (RE stimulators) to cholesterol-fed rabbits induced identical pattern of changes in cholesterol, phospholipid and triglyceride levels of the blood. However, the incidence of atheroma index in aorta and coronary arteries were significantly higher in histamine-treated and glycerol-trioleate-treated animals compared to cholesterol-fed controls. The rise in these indices appeared to be only partly related to increase in serum beta-lipoproteins but mostly due to increased permeability of the endothelium and internal elastic lamina probably caused by histamine phosphate and glycerol trioleate resulted in greater degree of atheromatous lesions in those groups.

Animals↗
PubMed1975

Lipid profile in the evolution of experimental atherosclerotic plaques from thrombus.

Nonocclusive white mural thrombosis was induced in the abdominal aortae of normolipidemic rabbits by insertion of a polyethylene catheter into the abdominal aortae. The thrombus subsequently organized into intimal thickenings which resembled fibrofatty type atherosclerosis seen in man, showing large numbers of foam cells containing stainable lipid, fatty necrotic centers, cholesterol clefts, calcification, and fibrous caps. The lipid composition of the thrombus and lesions was followed at serial time intervals from 4 hours to 60 weeks. Lipid analysis showed significant concentrations of lipid in the early lesions and with time these lipid concentrations increased and later decreased. These studies demonstrate that the fibrofatty lesions derived from a white thrombus have significant amounts of the same lipids that characterize the atherosclerotic lesions of man, however, there is a lower proportion of cholesterol to the other constituents and a higher proportion of phospholipids. The free cholesterol and cholesteryl ester of the 4-day lesions were much greater than that of platelets alone indicating that significant amounts of plasma are trapped in a thrombus when it forms.

Animals↗
PubMed1991

Phenotypic features of smooth muscle cells during the evolution of experimental carotid artery intimal thickening. Biochemical and morphologic studies.

Balloon catheter denudation of rat carotid artery that results in significant medial damage is followed by marked intimal smooth muscle cell (SMC) proliferation associated with limited endothelial regrowth. In this report we demonstrate that: (a) SMC of the carotid media, preceding their intimal proliferation, develop a cytoskeletal profile and morphology consistent with a de-differentiated SMC phenotype; and (b) both medial and intimal SMC subsequently revert to a cytoskeletal profile and morphology reflecting incomplete but significant re-differentiation toward normal SMC phenotype. Specifically, early after balloon injury, SMC of the media and those that have migrated into the intima contain decreased amounts of actin, desmin, and tropomyosin and increased amounts of vimentin; moreover, beta-actin becomes the dominant actin isoform, whereas alpha-actin decreases as compared with that found in normal medial SMC. Late after balloon injury, actin is still less abundant, however, desmin, tropomyosin, and vimentin return toward normal values and both medial and intimal SMC again show a predominance of alpha-actin, although the endothelium does not regenerate over the central surface of intimal thickening in this model. The SMC surface to volume ratio significantly decreases early after balloon injury, whereas it is not significantly different late after balloon injury as compared with that of SMC of the normal carotid media. We demonstrate, furthermore that: (c) adjacent luminal SMC are interconnected by gap junctions and develop focal tight junctions, a feature not reported previously to occur in smooth muscle; these cells however do not form any well defined membrane specialization with the leading edge of endothelium, supporting the view that presence of modified SMC on the luminal surface of chronically denuded vessels is not responsible for the cessation of endothelial regrowth.

Actins↗