title: Sonodynamic therapy decreased neointimal hyperplasia after stenting in the rabbit iliac artery.
abstract: BACKGROUND
  In-stent restenosis remains a pivotal problem after coronary and peripheral stenting. Sonodynamic therapy inhibits tumor growth by means of cytotoxicity after the activation of sonochemical sensitizers by ultrasound. PAD-S31 is known to be a water-soluble, chlorin-derivative sonochemical sensitizer. We assessed the efficacy of sonodynamic therapy using this sensitizer on neointimal hyperplasia in a rabbit stent model.
  
  
  RESULTS
  Stents were implanted in the iliac arteries of 16 rabbits. A total of 32 stented arteries were randomized to sonodynamic therapy, control, ultrasound exposure, and PAD-S31 groups. One hour after the intravenous administration of PAD-S31 (25 mg/kg body weight), ultrasound energy (1 MHz, 0.3 W/cm(2)) was delivered transdermally to the sonodynamic therapy group. At 28 days, all stent sites were analyzed morphometrically. The size of the intimal cross-sectional area was smaller in the sonodynamic therapy group than in the control, ultrasound, and PAD-S31 groups (0.31+/-0.07 versus 1.38+/-0.47, 1.66+/-0.71, and 1.61+/-0.42 mm(2), respectively; P<0.05). The ratio of the intimal and medial cross-sectional area was smaller in the sonodynamic therapy group than in the control, ultrasound, and PAD-S31 groups (0.71+/-0.22 versus 2.53+/-1.39, 2.48+/-0.60, and 3.45+/-1.42 mm(2); P<0.05).
  
  
  CONCLUSIONS
  Sonodynamic therapy with PAD-S31 is considered to be a feasible treatment modality for noninvasively inhibiting neointimal hyperplasia in a rabbit iliac stent model.
authors.affiliation: Internal Medicine I, National Defense Medical College, Saitama, Japan. karakawa@me.ndmc.ac.jp
authors.forename: Koh
authors.initials: K
authors.lastname: Arakawa
authors.forename: Kousukue
authors.initials: K
authors.lastname: Hagisawa
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kusano
authors.forename: Satoru
authors.initials: S
authors.lastname: Yoneyama
authors.forename: Akira
authors.initials: A
authors.lastname: Kurita
authors.forename: Tsunenori
authors.initials: T
authors.lastname: Arai
authors.forename: Makoto
authors.initials: M
authors.lastname: Kikuchi
authors.forename: Isao
authors.initials: I
authors.lastname: Sakata
authors.forename: Shin-ichirou
authors.initials: S
authors.lastname: Umenura Si
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Ohsuzu
mesh_terms: D000818:Animals; D003131:Combined Modality Therapy; D006083:Graft Occlusion, Vascular / Q000209:etiology / Q000473:pathology / Q000628:therapy*; D006965:Hyperplasia / Q000209:etiology / Q000473:pathology / Q000628:therapy; D007083:Iliac Artery / Q000473:pathology; D011166:Porphyrins / Q000627:therapeutic use; D011817:Rabbits; D015607:Stents / Q000009:adverse effects*; D014464:Ultrasonic Therapy / Q000379:methods*
chemical_list: C446480:13,17-bis(1-carboxypropionyl)carbamoylethyl-3-ethenyl-8-ethoxyiminoethylidene-7-hydroxy-2,7,12,18-tetramethyl porphyrin; D011166:Porphyrins