Objective To investigate the experience of left ventricular reconstruction（LVR）in a rat model with post-infarction ventricular aneurysm. Methods A total of 35 male Sprague-Dawley （SD）rats underwent left anterior descending artery （LAD） ligation to create a left ventricular aneurysm （LVA) model following myocardial infarction. Four weeks later, 16 rats with LVA that met the inclusion criteria underwent LVR as the experiment group（LVR group）. Another 10 rats with LVA underwent thoracotomy as the control group. Three days, 2 weeks, and 4 weeks after the second operation, all the rats were examined by echocardiography to evaluate the cardiac function. At the end of the study, photography and Masson’s Trichrome staining were used to evaluate the completeness of LVA resection. Results The surgical mortality of LVA and LVR generation was 11.4%（4/35）and 18.8%（3/16）respectively， with the success rate 74.3% （26/35）for LVA model and 81.3%（13/16）for LVR model. Photography and Masson’s Trichrome staining identified complete replacement of ventricular scar by patch. Three days after the second operation, echocardiography illustrated that the left ventricular end-systolic diameter （LVESD）and fractional shortening （FS） of the LVR group were significantly improved compared with the control group （LVESD 5.00±0.87 mm versus 5.90±0.92 mm, P＜0.05，FS 34.20%± 6.80% versus 26.60%±6.12%, P＜ 0.01）. The cardiac structure and function of LVR group were also significantly improved 2 weeks and 4 weeks after the second operation compared with the control group（2 weeks：left ventricular end-diastolic diameter （LVEDD）7.60±0.56 mm versus 8.50±1.08 mm，P＜ 0.01；LVESD 5.10±0.65 mm versus 6.69±0.89 mm，P＜0.001；FS 31.90%±6.90% versus 21.10%±6.17%，P＜0.001；4 weeks：LVEDD7.70±0.50 mm versus 9.10±0.89 mm，P＜0.001；LVESD5.20±0.39 mm versus 7.20±0.95 mm，P＜0.001；FS 31.80%±2.40% versus 20.20%±4.17%，P＜0.001）. Conclusions LVR rat can be used as a stable, reliable and economic screeningmodel in engineered heart tissue（EHT）research.
Objective To observe the impact of collagen patches using 1-ethyl-3- （3-dimethylaminopropyl) carbod-iimide hydrochloride chemistry （EDC） to conjugate vascular endothelial growth factor （VEGF） ＋ basic fibroblast growth factor （bFGF） or VEGF alone on the survival rate of transplanted human bone morrow mesenchymal stem cells （hBM-MSCs）in vitro and in vivo. Methods Collagen patches which were activated by EDC were used as the control group，and EDC activated collagen patches that were conjugated with VEGF or VEGF ＋ bFGF were used as the experiment groups（VEGF group and VEGF ＋ bFGF group）. hBM-MSCs （0.5×106/patch） were used as seeding cells to construct engineered heart tissue （EHT）. MTT assay was performed to assess in vitro proliferation of hBM-MSCs on 3 different collagen patches. Ventricular aneurysm model after myocardial infarction was created by left anterior descending artery （LAD） ligation in male SD rats，and EHT which were constructed with 3 different patches were used for ventricular plasty. Four weeks later，immunofluorescence staining was used to examine arteriole density （anti-α-SMA staining） and transplanted cell survival （anti-h-mitochondria staining）. Results （1） hMSCs proliferation in VEGF group and VEGF ＋ bFGF group was significantly better than that in the control group on the 2nd and 4th day after cell transplantation （P＜0.05）； （2） Four weeks afterEHT implantation，immunofluorescence staining for α-SMA revealed that arteriole density of VEGF group and VEGF ＋ bFGF group was significantly higher than that of the control group （P＜0.05）； （3） Immunofluorescence staining forh-mitochondria showed that survival rates of transplanted hBM-MSCs of VEGF group and VEGF ＋ bFGF group were significantly higher than that of the control group （P＜0.05）； （4） There was a significantly positive correlation between survival rate of hBM-MSCs and arteriole density （r 2=0.99，P=0.02）. Conclusion VEGF or VEGF ＋ bFGF conjugated collagen patch can significantly improve hBM-MSCs proliferation in vitro and enhance survival rate of transplanted hBM-MSCs by accelerating revascularization of EHT in vivo.