title: Perivascular inflammation after balloon angioplasty of porcine coronary arteries.
abstract: BACKGROUND
  Inflammation has been suggested to play a role in vascular lesion formation after angioplasty. Whereas previous studies have focused on inflammatory reactions in the intima and media, less attention has been paid to adventitial and perivascular responses and their potential role in vascular remodeling.
  
  
  RESULTS
  Balloon overstretch injury of porcine coronary arteries was performed with standard clinical angioplasty catheters. Vessels were examined from 0.5 hour to 14 days after injury by immunohistochemistry and in situ hybridization (ISH) for neutrophil and macrophage markers, cell adhesion molecules (P-selectin, E-selectin, and vascular cell adhesion molecule-1), and neutrophil-specific CXC chemokines (alveolar macrophage-derived neutrophil chemotactic factor [AMCF]-I/interleukin-8 and AMCF-II). Neutrophils accumulated in the adventitia surrounding the injury site from 2 hours to 3 days, followed by macrophages from 1 to 7 days after angioplasty. Inflammation was associated temporally with the expression of mRNAs encoding cell adhesion molecules and chemokines. The main inflammatory and proliferative foci were not limited to the adventitia but rather extended many millimeters away from the injured vessel throughout the surrounding adipose and myocardial tissues.
  
  
  CONCLUSIONS
  Inflammatory responses after angioplasty of porcine coronary arteries occurred throughout the entire perivascular tissue. We hypothesize that perivascular inflammatory cells play a role in the recruitment and/or proliferation of adventitial myofibroblasts, possibly through the release of reactive oxygen species and/or cytokines, and thus contribute to vascular remodeling associated with postangioplasty restenosis.
authors.affiliation: Winship Cancer Institute, Department of Surgery, Emory University, Atlanta, GA, USA.
authors.forename: E
authors.initials: E
authors.lastname: Okamoto
authors.forename: T
authors.initials: T
authors.lastname: Couse
authors.forename: H
authors.initials: H
authors.lastname: De Leon
authors.forename: J
authors.initials: J
authors.lastname: Vinten-Johansen
authors.forename: R B
authors.initials: RB
authors.lastname: Goodman
authors.forename: N A
authors.initials: NA
authors.lastname: Scott
authors.forename: J N
authors.initials: JN
authors.lastname: Wilcox
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D002452:Cell Count; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D004195:Disease Models, Animal; D005260:Female; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007249:Inflammation / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D007962:Leukocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D020556:Neutrophil Infiltration; D009195:Peroxidase / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000235:genetics / Q000378:metabolism; D013552:Swine
chemical_list: D015815:Cell Adhesion Molecules; D018925:Chemokines; D012333:RNA, Messenger; D009195:Peroxidase; D016186:Receptor, Macrophage Colony-Stimulating Factor