Papers

International journal
Jun, 2008

Invasion of atheromatous plaques into tunica media causes coronary outward remodeling in WHHLMI rabbits

ATHEROSCLEROSIS
  • Masashi Shiomi
  • ,
  • Satoshi Yamada
  • ,
  • Akihiro Matsukawa
  • ,
  • Hiroyuki Itabe
  • ,
  • Takashi Ito

Volume
198
Number
2
First page
287
Last page
293
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1016/j.atherosclerosis.2008.02.010
Publisher
ELSEVIER IRELAND LTD

To clarify the mechanism of coronary outward remodeling, we examined atherosclerotic coronary arteries morphologically using WHHLMI rabbits that develop coronary atherosclerosis spontaneously. Perfusion-fixed coronary segments of WHHLMI rabbits were prepared at 500 mu m intervals. After immunohistochemical staining and histopathological staining, the areas and lengths of the arterial wall and the lesions were measured. Obvious outward remodeling was observed in coronary sections with greater than 40% cross-sectional narrowing. In coronary sections with greater than 40% cross-sectional narrowing, the tunica media was thick at the shoulder of atheromatous plaque and was thin beneath the atheromatous plaques. Macrophages infiltrated those attenuated tunica media expressed matrix metalloproteinases and oxidized LDL was accumulated in those areas. In those areas, collagen fibers and the internal elastic lamina had disappeared partly and apoptotic smooth muscle cells were observed. Proliferation of smooth muscle cells was observed at the attenuated tunica media and adjacent adventitia. The present results suggest that invasion of atheromatous plaques into the tunica media causes coronary outward remodeling. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

Link information
DOI
https://doi.org/10.1016/j.atherosclerosis.2008.02.010
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/18394628
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000257133600006&DestApp=WOS_CPL
ID information
  • DOI : 10.1016/j.atherosclerosis.2008.02.010
  • ISSN : 0021-9150
  • Pubmed ID : 18394628
  • Web of Science ID : WOS:000257133600006

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