ISSN:
1619-7089
Keywords:
Atheromatous plaque
;
Atherosclerosis
;
Indium-111 labelled immunoglobulin Gc
;
Iodine-125 labelled low-density lipoprotein
;
Iodine-125 labelled endothelin-1
;
Balloon de-endothelialization
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract To test iodine-125 labelled low-density lipoprotein (125I-LDL), polyclonal indium-111 labelled immunoglobulin G (111In-IgG) and iodine-125 labelled endothelin-1 uptake in metabolically active atheromatous plaques after arterial wall injury, we performed balloon de-endothelialization of carotid arteries or abdominal aortas in 24 New Zealand male rabbits which were fed with a normal diet (n=14) or a hypercholesterolaemic diet (n=10) after surgery. Six weeks later the animals were injected with 200 μCi of (125I-LDL), and/or with 100 μCi of 111In-IgG or with 9 μCi of 125I-endothelin-1. Forty-eight hours later the animals were sacrificed. Carotid arteries and aortas were removed, counted and fixed for autoradiography and light microscopy examination. Contralateral carotid arteries and thoracic aortas served as controls. Significant 111In-IgG uptake was observed in the injured arteries at autoradiography, with localization mainly in the healing edges, and at well counting. The percentage of the injected dose per gram (%D.inj/g) was 0.0188±0.06 versus 0.0059±0.003 in controls (P〈 0.05). There was no difference in 111In-IgG uptake between arteries with injury alone and those with active atheroma formation at the site of the injury. Significant (125I-LDL), uptake was observed only when lipid deposition was present at light microscopy (%D.inj/g of 0.0024±0.0005 vs 0.0010±0.0003 in controls, P 〈 0.05). 125I-endothelin-1 accumulation was observed in four of five injured aortas both at autoradiography, with diffuse localization, and at well counting (%D.inj/g of 0.0012±0.0004 in the abdominal aortas vs 0.0008±0.0003 in the thoracic aortas). Polyclonal IgG may accumulate in injured arteries without active atheroma formation. Inflammatory reaction at the site of the injury may cause 111In-IgG uptake independently of atheromatous plaque formation. LDL accumulation takes place only with active atheroma formation at the site of the injury. Use of labelled peptides such as endothelin-1 may provide further insight into the mechanisms of atheromatous plaque formation.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00171011
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