Experimental calcification of the aorta in rabbits: Effects of chelating agents and glucagon

C Cavallotti, F M Tranquilli Leali, M Artico, V D'Andrea, V Malinovska
2014
Experimental calcification of the aorta, induced in rabbits by a single dose of 8 mg of dihydro-tachysterol (AT 10), represents an optimal model for studying vascular diseases caused by lipid and calcium deposition on the artery wall. This lesion may be treated with chelating agents and/or with glucagon. The effect of chelating agents and/or of glucagon on lipid and calcium deposition involving the aortic wall was studied in 12 adult white Flemish rabbits. The animals were divided into four
more » ... ps and in each of them experimental calcification of the aorta was induced by AT 10. The first group did not receive any treatment and served as control. The second group received only ethylenediamine tetraacetic acid (EDTA) (120 mg daily). The third group received only glucagon (0.1 mg subcutaneously). In the fourth group, the glucagon (0.1 mg subcutaneously) was injected with EDTA (120 mg daily). The animals were killed 30 days after suspension of therapy. The aorta was rapidly harvested in its thoracic tract. The calcium content of the sclerosed aorta was determined by flame photometer, while the cytochemical detection of calcium was performed using N,N-Naphthaloyl-hydroxyl-amine. Lipid deposition was studied by Sudan black B staining. Usual laboratory staining (hematoxyline - eosine and Toluidin blue ) were used for detection of structural details. All morphological results were submitted to the quantitative analysis of images and statistical analysis. The results of the present study suggest that glucagon may play a role in the biochemical and morphological modifications usually found in atherosclerosis. In fact, macroscopic and ultrastructural evaluation of our morphological results suggest that the pathological changes observed may be restored by administration of glucagons and/or by chelating therapy.
doi:10.23675/sjlas.v31i4.71 fatcat:awowgurlfrds5kskf5mpaehjyq