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Research Article Free access | 10.1172/JCI113368

Aneurysm of the rabbit common carotid artery induced by periarterial application of calcium chloride in vivo.

S D Gertz, A Kurgan, and D Eisenberg

Department of Anatomy, Hebrew University, Jerusalem, Israel.

Find articles by Gertz, S. in: JCI | PubMed | Google Scholar

Department of Anatomy, Hebrew University, Jerusalem, Israel.

Find articles by Kurgan, A. in: JCI | PubMed | Google Scholar

Department of Anatomy, Hebrew University, Jerusalem, Israel.

Find articles by Eisenberg, D. in: JCI | PubMed | Google Scholar

Published March 1, 1988 - More info

Published in Volume 81, Issue 3 on March 1, 1988
J Clin Invest. 1988;81(3):649–656. https://doi.org/10.1172/JCI113368.
© 1988 The American Society for Clinical Investigation
Published March 1, 1988 - Version history
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Abstract

Experimental aneurysmatic dilatation of the rabbit common carotid artery was induced by a single, periarterial application of calcium chloride in vivo. Vessels were fixed in situ after 3 d, 1 wk, 3 wk, 6 wk, and 12 wk by intracardiac perfusion of glutaraldehyde and tissues prepared for light, scanning, and transmission electron microscopy. Progressive focal aneurysmal dilatation was seen limited to the site of calcium application with endothelial damage and thrombus formation in areas of irregular luminal contour. Disruption of the elastic network of the intima and media was seen with varying degrees of intimal fibromuscular hyperplasia and medial disorganization. The calcium-elastic tissue complex was the focus of the inflammatory, arteriosclerotic reaction and subsequent aneurysm formation. The inflammatory cell infiltration initially included primarily neutrophils followed by lymphocytes, plasma cells, monocytes, and multinucleated giant cells. These studies support the hypothesis that disruption of the elastic tissue network of the vascular wall represents an important pathogenetic factor in the initiation of aneurysmal dilatation. In addition, the results of these studies suggest that interaction of calcium with the elastica of the arterial wall may represent an important pathogenetic factor in the initiation of giant cell arteritis.

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