title: Reduction of thrombus formation without inhibiting coagulation factors does not inhibit intimal hyperplasia after balloon injury in pig coronary arteries.
abstract: BACKGROUND
  The proposed mechanisms of restenosis after coronary angioplasty include neointima formation, vessel wall remodeling and mural thrombus. Poloxamer 188 does not inhibit coagulation factors, but was shown to reduce mural thrombus formation in pig coronary arteries after intracoronary stenting in an acute study. This study was performed to examine whether this agent may reduce neointima formation.
  
  
  METHODS
  Thirty domestic juvenile pigs of weight 20-30 kg were anesthetized. A left angiogram was performed via a femoral artery. Proximal left anterior descending and circumflex arteries were dilated three times with a 20-30% oversized coronary angioplasty balloon catheter. Fifteen animals were allocated randomly to receive intravenous infusions of poloxamer 188, starting 30 min before angioplasty and continuing for 24 h. The remaining 15 received intravenous 0.45% saline and served as controls. The animals were killed 2 weeks after the angioplasty. Histologic studies of the arteries were performed. The severity of the injury and the amount of thrombus material incorporated in the neointima were assessed by semiquantitative methods.
  
  
  RESULTS
  There was no significant difference between injury scores in the two groups. Thrombus material in the neointima in the treatment group was significantly less than that in those of the control group (thrombus areas 0.013 +/- 0.004 compared with 0.029 +/- 0.006 mm2, P < 0.02), but there were no significant differences between the neointimal (0.60 +/- 0.08 and 0.60 +/- 0.13 mm2) and luminal (2.51 +/- 0.21 and 2.44 +/- 0.26 mm2) areas in treatment and control groups.
  
  
  CONCLUSIONS
  Continuous 24 h intravenous infusion of poloxamer 188 after balloon injury in pig coronary arteries may reduce mural thrombus formation significantly, but did not reduce neointima formation.
authors.affiliation: Department of Medicine, University of Alabama at Birmingham 35294, USA.
authors.forename: M W
authors.initials: MW
authors.lastname: Liu
authors.forename: J A
authors.initials: JA
authors.lastname: Hearn
authors.forename: J F
authors.initials: JF
authors.lastname: Luo
authors.forename: P G
authors.initials: PG
authors.lastname: Anderson
authors.forename: G S
authors.initials: GS
authors.lastname: Roubin
authors.forename: S
authors.initials: S
authors.lastname: Iyer
authors.forename: L
authors.initials: L
authors.lastname: Bilodou
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D001779:Blood Coagulation Factors / Q000187:drug effects*; D003328:Coronary Thrombosis / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D003331:Coronary Vessels / Q000187:drug effects / Q000293:injuries / Q000473:pathology*; D004195:Disease Models, Animal; D005343:Fibrinolytic Agents / Q000008:administration & dosage; D006965:Hyperplasia; D007262:Infusions, Intravenous; D011060:Poloxalene / Q000008:administration & dosage; D011897:Random Allocation; D013552:Swine; D015912:Thrombolytic Therapy / Q000379:methods*; D017539:Tunica Intima / Q000187:drug effects / Q000293:injuries / Q000473:pathology*
chemical_list: D001779:Blood Coagulation Factors; D005343:Fibrinolytic Agents; D011060:Poloxalene