Shock wave-pretreated bone marrow cells further improve left ventricular function after myocardial infarction in rabbits

Ann Vasc Surg. 2010 Aug;24(6):809-21. doi: 10.1016/j.avsg.2010.03.027.

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.

Methods and 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Marrow Cells / radiation effects*
  • Bone Marrow Transplantation*
  • Cells, Cultured
  • Connexin 43 / metabolism
  • Cytochromes c / metabolism
  • Disease Models, Animal
  • Endothelin-1 / genetics
  • Fibrosis
  • Gene Expression Regulation
  • High-Energy Shock Waves*
  • Male
  • Matrix Metalloproteinase 9 / genetics
  • Mitochondria, Heart / metabolism
  • Myocardial Infarction / diagnosis
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / physiopathology
  • Myocardial Infarction / surgery*
  • Myocardium / metabolism
  • Myocardium / pathology
  • Nitric Oxide Synthase Type III / genetics
  • Oxidative Stress
  • RNA, Messenger / metabolism
  • Rabbits
  • Recovery of Function
  • Time Factors
  • Transplantation, Autologous
  • Ventricular Function, Left*

Substances

  • Connexin 43
  • Endothelin-1
  • RNA, Messenger
  • Cytochromes c
  • Nitric Oxide Synthase Type III
  • Matrix Metalloproteinase 9