title: Shock wave-pretreated bone marrow cells further improve left ventricular function after myocardial infarction in rabbits.
abstract: BACKGROUND
  We tested whether shock wave (SW) offers additional benefits in improving left ventricular (LV) function after acute myocardial infarction (AMI) in rabbits receiving SW-treated autologous bone marrow-derived mononuclear cells (BMDMNCs) transplantation.
  
  
  RESULTS
  Saline (750 microL; group 2), BMDMNCs (1.0 x 10(7); group 3), or preimplant SW-treated BMDMNCs (group 4) were implanted into the infarct area of male rabbits 15 minutes after left coronary artery ligation, whereas eight rabbits without AMI served as controls (group 1; n = 8 per group). The results showed that in infarct area of LV, protein expressions of Cx43 and cytochrome C in mitochondria and endothelial nitric oxide synthase mRNA expression were lower in group 2 than in other groups, and decreased in group 3 as compared with groups 1 and 4 (all p values < 0.01). Conversely, mRNA expressions of endothelin-1 and matrix metalloproteinase-9, mitochondrial oxidative stress, and total fibrotic area were higher in group 2 than in other groups (all p values < 0.05). Furthermore, 6-month LV function by 2-D echo/angiogram showed significant impairment in group 2 than in other groups and in group 3 than in groups 1 and 4 (all p values < 0.005).
  
  
  CONCLUSIONS
  Application of SW-treated autologous BMDMNCs is superior to BMDMNCs alone for preserving LV function after AMI.
authors.affiliation: Division of Cardiovascular and Thoracic Surgery, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan, ROC.
authors.forename: Jiunn-Jye
authors.initials: JJ
authors.lastname: Sheu
authors.forename: Cheuk-Kwan
authors.initials: CK
authors.lastname: Sun
authors.forename: Li-Teh
authors.initials: LT
authors.lastname: Chang
authors.forename: Hsiu-Yu
authors.initials: HY
authors.lastname: Fang
authors.forename: Sheng-Ying
authors.initials: SY
authors.lastname: Chung
authors.forename: Sarah
authors.initials: S
authors.lastname: Chua
authors.forename: Morgan
authors.initials: M
authors.lastname: Fu
authors.forename: Fan-Yen
authors.initials: FY
authors.lastname: Lee
authors.forename: Ying-Hsien
authors.initials: YH
authors.lastname: Kao
authors.forename: Sheung-Fat
authors.initials: SF
authors.lastname: Ko
authors.forename: Ching-Jen
authors.initials: CJ
authors.lastname: Wang
authors.forename: Chia-Hung
authors.initials: CH
authors.lastname: Yen
authors.forename: Steve
authors.initials: S
authors.lastname: Leu
authors.forename: Hon-Kan
authors.initials: HK
authors.lastname: Yip
mesh_terms: D000818:Animals; D001854:Bone Marrow Cells / Q000528:radiation effects*; D016026:Bone Marrow Transplantation; D002478:Cells, Cultured; D018031:Connexin 43 / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000235:genetics; D005355:Fibrosis; D005786:Gene Expression Regulation; D019220:High-Energy Shock Waves; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000235:genetics; D008929:Mitochondria, Heart / Q000378:metabolism; D009203:Myocardial Infarction / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D052250:Nitric Oxide Synthase Type III / Q000235:genetics; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D020127:Recovery of Function; D013997:Time Factors; D014182:Transplantation, Autologous; D016277:Ventricular Function, Left
chemical_list: D018031:Connexin 43; D019332:Endothelin-1; D012333:RNA, Messenger; D045304:Cytochromes c; D052250:Nitric Oxide Synthase Type III; D020780:Matrix Metalloproteinase 9