Article

Inflammation

, Volume 35, Issue 4, pp 1530-1537

First online:

Lipopolysaccharide-Induced Proliferation of the Vasa Vasorum in a Rabbit Model of Atherosclerosis as Evaluated by Contrast-Enhanced Ultrasound Imaging and Histology

  • Jinwei TianAffiliated withKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Department of Cardiology, Second Affiliated Hospital of Harbin Medical University
  • , Sining HuAffiliated withKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Department of Cardiology, Second Affiliated Hospital of Harbin Medical University
  • , Xue HanAffiliated withDepartment of Ultrasound, Third Affiliated Hospital of Harbin Medical University
  • , Nana DongAffiliated withKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Department of Cardiology, Second Affiliated Hospital of Harbin Medical University
  • , Huai YuAffiliated withKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Department of Cardiology, Second Affiliated Hospital of Harbin Medical University
  • , Yanli SunAffiliated withKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Department of Cardiology, Second Affiliated Hospital of Harbin Medical University
  • , Bo YuAffiliated withKey Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Department of Cardiology, Second Affiliated Hospital of Harbin Medical University Email author 

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Abstract

Whether lipopolysaccharide (LPS) can promote vasa vasorum (VV) proliferation for atherosclerosis in vivo is unclear. Eighteen rabbits with atherosclerosis were randomly assigned into one of three groups of six. Group A received biweekly injections of 10 mL saline after 2 weeks of balloon injury. Groups B and C received biweekly intravenous injections of 3.0 μg LPS in 10 mL saline at weeks 10 and 4, respectively, until study termination. LPS significantly increased the levels of triglycerides and C-reactive protein and decreased the level of high-density lipoprotein cholesterol. Group C had significant larger plaques and more macrophages than group A (p = 0.01 and p < 0.001, respectively). Contrast enhancement ultrasound imaging and histological detection demonstrated that plaques in group C had a significantly higher VV density than that in group A (p = 0.009 and p = 0.002, respectively). In summary, VV proliferation for plaque destabilization can be accelerated by LPS-induced systemic inflammation and changes in lipid profiles.

KEY WORDS

atherosclerosis contrast enhancement ultrasound inflammation lipopolysaccharide vasa vasorum