The cost of publication in Journal of Biomedical Science is borne by the National Science Council, Taiwan.
Research
Developing a novel rabbit model of atherosclerotic plaque rupture and thrombosis by cold-induced endothelial injury
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* Corresponding authors: Shun-Miao Fang doctorfsm2006@yahoo.com.cn - Qing-Hua Zhang zqh504020@yahoo.com.cn
1 Department of Cardiology, Southern Medical University (SMF), Guangzhou, 510515, China
2 Experimental Centre, the 305 Hospital of Chinese People's Liberation Army (QHZ, ZXJ), Beijing, 100017, PR China
Journal of Biomedical Science 2009, 16:39 doi:10.1186/1423-0127-16-39
Published: 4 April 2009Abstract
Background
It is widely believed that atherosclerotic plaque rupture and subsequent thrombosis leads to acute coronary events and stroke. However, study of the mechanism and treatment of human plaque rupture is hampered by lack of a suitable animal model. Our aim was to develop a novel animal model of atherosclerotic plaque rupture to facilitate the study of human plaque disruption and thrombosis.
Methods
28 healthy male New Zealand white rabbits were randomly divided into two groups: rabbits in group A (n = 12) were only fed a high-fat diet for eight weeks; rabbits in group B (n = 16) underwent cold-induced endothelial injury with liquid nitrogen, then were given a high-fat diet for eight weeks. After completion of the preparatory regimen, triggering of plaque rupture was attempted by local injection of liquid nitrogen in both groups.
Results
All rabbits in group B had disrupted plaques or rupture-driven occlusive thrombus formation, but none in group A showed any effects. More importantly, the cold-induced plaques in our model were reminiscent of human atherosclerotic plaques in terms of architecture, cellular composition, growth characteristics, and patterns of lipid accumulation.
Conclusion
We successfully developed a novel rabbit model of atherosclerotic plaque rupture and thrombosis, which is simple, fast, inexpensive, and reproducible, and has a low mortality and a high yield of triggering. This model will allow us to better understand the mechanism of human plaque rupture and also to develop plaque-stabilizing therapies.