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Vascular effects of diet-induced hypercalcemia after balloon artery injury in giant Flemish rabbits

To determine whether metastatic calcification during neointima formation can result in neointimal calcification that simulates advanced human atherosclerosis, 32 giant Flemish rabbits (weight 5.5 ± 0.6 kg) underwent overstretch balloon injury of bilateral iliac arteries and received diet therapy for...

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Published in:The American heart journal 1995-10, Vol.130 (4), p.758-764
Main Authors: Hong, Mun K., Vossoughi, Jafar, Haudenschild, Christian C., Wong, S.Chiu, Zuckerman, Bram D., Leon, Martin B.
Format: Article
Language:English
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Summary:To determine whether metastatic calcification during neointima formation can result in neointimal calcification that simulates advanced human atherosclerosis, 32 giant Flemish rabbits (weight 5.5 ± 0.6 kg) underwent overstretch balloon injury of bilateral iliac arteries and received diet therapy for 8 weeks: high cholesterol (2%) and low calcium—vitamin D 2 regimen (250 mg of calcium carbonate orally 5 times weekly and 50,000 U of calciferol intramuscularly 3 times weekly; group 1; n = 5); low cholesterol (0.5%) and high calcium—vitamin D 2 regimen (500 mg of calcium carbonate orally 5 times weekly and 100,000 U of calciferol intramuscularly three times weekly; group 2; n = 19); or 0% cholesterol and high calcium—vitamin D 2 regimen (group 3; n = 8). The incidence of vascular calcification was highest (71.4%) in group 2. Eighty-one percent of calcification was medial. Residual strain measurements of 7 thoracic aortas from group 2 compared to normal thoracic aortas from 8 control rabbits showed that residual strain was significantly increased in the calcified atherosclerotic aortas (12.3% vs 5.2%; p = 0.001). We conclude that diet-induced hypercalcemia predominantly affects the media despite the presence of concomitant neointima formation from balloon artery injury with or without hypercholesterolemia and increases the residual strain more than twofold compared to normal thoracic aortas.
ISSN:0002-8703
1097-6744
DOI:10.1016/0002-8703(95)90074-8