Effects of autologous transplantation of bone marrow mononuclear cells on ventricular remodeling after myocardial infarction in swines
- VernacularTitle:小型猪自体骨髓单个核细胞移植对心肌梗死后心室重构的影响
- Author:
Xiaorong XU
;
Shangyu WEN
;
Wei GAO
- Publication Type:Journal Article
- Keywords:
Bone marrow cells;
Myocardial infarction;
Ventricular remodeling;
Stem cell transplantation
- From:
Chinese Journal of Interventional Cardiology
1993;0(02):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effects of bone marrow mononuclear cells (MNCs) transplantation on left ventricular (LV) remodeling and its potential mechanism in swine myocardial infarction models. Methods The left anterior descending coronary arteries of swines were obstructed by balloon to create myocardial infarction models. Three weeks later, MNCs(n= 7)or PBS(n=5) were injected into the infarction related coronary arteries through balloon catheter. The cardiac function were measured by echocardiography and ventriculargraphy. Collagen amount was also assessed at 4 weeks after transplantation. Results At 4 weeks after transplantation, LV end-diastolic dimension decreased in the BM-MNC group than before (40.40?4.51 mm vs. 45.88?4.15 mm, P=0.026), but increased in the control group (48.50?9.31 mm vs. 42.40?7.29 mm, P=0.328). Left ventricular function was improved from 41.16%?9.83% to 47.50%?9.07% in the BM-MNC group (P=0.020) but there was no significant change in the control group. Significant differences existed between the 2 groups in their absolute change before and after the procedure in both LV dimension and LV function (P=0.046 and P=0.030 respectively). The results showed reduction of collagen content in the border and the remote infarct regions in the BM-MNC group compared with the control (P=0.047 and P=0.034 respectively). Conclusion BM-MNCs transplantation regulates collagen content in heart and attenuates the degree of post-MI LV dilation and the development of infarction area. This effect of BM-MNCs transplantation may be one of the mechanisms which intervene ventricular remodeling following myocardial infarction.
