title: Extracorporeal low-energy shock-wave therapy exerts anti-inflammatory effects in a rat model of acute myocardial infarction.
abstract: BACKGROUND
  It has been previously demonstrated that extracorporeal low-energy shock-wave (SW) therapy ameliorates left ventricular (LV) remodeling through enhanced angiogenesis after acute myocardial infarction (AMI) in pigs in vivo. However, it remains to be examined whether SW therapy also exerts anti-inflammatory effects on AMI. METHODS AND RESULTS: AMI was created by ligating the proximal left anterior descending coronary artery in rats. They were randomly assigned to 2 groups: with (SW group) or without (control group) SW therapy (0.1 mJ/mm(2), 200 shots, 1 Hz to the whole heart at 1, 3 and 5 days after AMI). Four weeks after AMI, SW therapy significantly ameliorated LV remodeling and fibrosis. Histological examinations showed that SW therapy significantly suppressed the infiltration of neutrophils and macrophages at days 3 and 6, in addition to enhanced capillary density in the border area. Molecular examinations demonstrated that SW therapy enhanced the expression of endothelial nitric oxide synthase and suppressed the infiltration of transforming growth factor-β1-positive cells early after AMI. SW therapy also upregulated anti-inflammatory cytokines and downregulated pro-inflammatory cytokines in general.
  
  
  CONCLUSIONS
  These results suggest that low-energy SW therapy suppressed post-MI LV remodeling in rats in vivo, which was associated with anti-inflammatory effects in addition to its angiogenic effects, and demonstrated a novel aspect of the therapy for AMI.
authors.affiliation: Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine.
authors.forename: Yuzuru
authors.initials: Y
authors.lastname: Abe
authors.forename: Kenta
authors.initials: K
authors.lastname: Ito
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Hao
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Shindo
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Ogata
authors.forename: Yuta
authors.initials: Y
authors.lastname: Kagaya
authors.forename: Ryo
authors.initials: R
authors.lastname: Kurosawa
authors.forename: Kensuke
authors.initials: K
authors.lastname: Nishimiya
authors.forename: Kimio
authors.initials: K
authors.lastname: Satoh
authors.forename: Satoshi
authors.initials: S
authors.lastname: Miyata
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Kawakami
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Shimokawa
mesh_terms: D000818:Animals; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D005355:Fibrosis; D005786:Gene Expression Regulation; D007249:Inflammation; D008264:Macrophages / Q000502:physiology; D008297:Male; D009203:Myocardial Infarction / Q000276:immunology / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic; D020556:Neutrophil Infiltration; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013016:Sound; D013318:Stroke Volume; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000235:genetics; D020257:Ventricular Remodeling
chemical_list: D016207:Cytokines; D053773:Transforming Growth Factor beta1; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat