Inhibitory effect of fluvastatin on lysophosphatidylcholine-induced ventricular arrhythmias in rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of fluvastatin on lysophosphatidylcholine (LPC)-induced ventricular arrhythmias and its mechanism.</p><p><b>METHODS</b>Twenty male SD rats were randomly allocated into two equal groups, namely LPC treatment group and fluvastatin pretreatment group. Langendorff apparatus was used for cardiac perfusion ex vivo with 5 µmol/L LPC for 5 min followed by washing for 30 min in LPC treatment group, and in fluvastatin pretreatment group, a 30-min perfusion with 10 µmol/L fluvastatin was administered before LPC perfusion. The LPC-induced nonselective cation current (I(NSC)) in the ventricular myocytes was recorded using the whole-cell voltage-clamp method.</p><p><b>RESULTS</b>Fluvastatin significantly inhibited LPC-induced ventricular tachyarrhythmia/fibrillation and I(NSC). The small G-protein Rho inhibitor (C3) and Rho-kinase inhibitor (Y-27632) in the pipette solution also suppressed LPC-induced I(NSC).</p><p><b>CONCLUSION</b>Fluvastatin offers cardiac protection against LPC by inhibiting LPC-induced I(NSC). LPC induces fatal arrhythmia via a Rho/Rho-kinase-mediated pathway.</p>

Establishment of a rabbit model of congestive heart failure / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the feasibility of establishing a rabbit model of congestive heart failure model by abdominal aortic coarctation combined with intravenous epinephrine infusion.</p><p><b>METHODS</b>Twenty rabbits were randomized into the study group (n=10) and control group (n=10). Congestive heart failure was induced in the study group by abdominal aortic coarctation combined with intravenous epinephrine infusion. The diameter of the abdominal aorta was reduced by 50%-60%, and epinephrine was infused at 2 weeks (5 mg.kg(-1).min(-1) for 60 min), 4 weeks (4 mg.kg(-1).min(-1) for 60 min) and 6 weeks (4 mg.kg(-1).min(-1) for 60 min) after the operation. The changes in the systolic and diastolic functions of the rabbits were assessed by echocardiography and catheterization during the progression of left hypertrophy.</p><p><b>RESULTS</b>The diameter of the abdominal aorta at the coarctation region was 4.87-/+0.53 mm before the operation, reduced to 2.26-/+0.47 mm after the operation. At 8 weeks after the operation, the hearts of the rabbits in the study group showed obvious abnormalities in echocardiography, while the hearts in the control group remained normal.</p><p><b>CONCLUSION</b>Abdominal aortic coarctation combined with intravenous epinephrine infusion allows rapid establishment of a reliable rabbit model of chronic congestive heart failure.</p>

Study of the three-dimensional structure of the ventricular myocardial fiber in human heart / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the three-dimensional structure of ventricular myocardial fiber in human heart.</p><p><b>METHODS</b>Eight human heart were obtained from male donors aged 81.9-/+7.2 years with a heart weight of 455.6-/+65.7 g. Each sample was immersed in water and scanned by diffusion tensor magnetic resonance imaging (DT-MRI) using a 3 Tesla Exicte HD by an eight-channel head coils. The duration was 18.6-/+5.2 h from heart arresting to the scanning. The data were obtained using the protocol of single shot echo planar imaging (sshEPI) and sensitivity encoding (SENSE). The SENSE-sshEPI-scans (TE/TRZ86.4/2000 ms) of the whole heart were carried out (b=1000 s/mm(2), voxels 128x128, resolution 1.1 mmx1.1 mmx(3) mm, and FOV 14 cmx14 cm). Fiber tracking and reconstruction were performed using GE Advantage Windows Workstation. The three-dimensional structure of the ventricular myocardial fiber was observed.</p><p><b>RESULTS</b>The left ventricular myocardial fibers showed two layers with different directions of alignment in such regions as the anterior, septum, and posterior walls and the free left ventricular wall. The subendocardial layer ran obliquely from the base to the apex, and the middle layer ran obliquely upward from the base to the apex. The two layers were linked together and aligned in the pattern of helical coils near the apex.</p><p><b>CONCLUSIONS</b>The three-dimensional structure of the myocardial fibers in human heart conforms to Torrent's hypothesis of helical ventricular myocardial band (HVMB).</p>

Effects of pravastatin and granulocyto-colony stimulating factor in mobilizing endothelial progenitor cells in mice with myocardial ischemia / 南方医科大学学报

<p><b>OBJECTIVE</b>To compare the effects of pravastatin and granulocyto-colony stimulating factor (G-CSF) in mobilizing endothelial progenitor cells (EPCs) in mice with myocardial ischemia, and explore the possible mechanism of EPC mobilization.</p><p><b>METHODS</b>Ninety-six mice were randomly divided into 4 groups (n=24), namely the control group, saline group, pravastatin group and G-CSF group. In the latter 3 groups, myocardial ischemia was induced with isoprenine followed by intraperitoneal injections of normal saline, pravastatin and G-CSF for 5 consecutive days. On days 1, 5, 7, and 9 after establishment of myocardial ischemia, 6 mice from each group were randomly selected for measurement of the EPC count and serum concentrations of vascular endothelial growth factor (VEGF).</p><p><b>RESULTS</b>Compared with the control group, EPC count increased slightly in the saline group on days 1, 5, and 7. EPC count increased significantly in pravastatin group on days 5, 7 and 9 in comparison with that of the saline group, and the increment was more obvious in G-CSF group. In comparison with the control group, the concentrations of VEGF augmented on days 5, 7 and 9 in the order of saline group, pravastatin group and G-CSF group. The effect of G-CSF on EPC mobilization was positively correlated to VEGF concentrations.</p><p><b>CONCLUSION</b>Myocardial ischemia induces EPC mobilization and VEGF release. Both Pravastatin and G-CSF can enhance EPC mobilization from the bone marrow and VEGF release, but G-CSF produces a stronger effect on EPC mobilization in association of VEGF release.</p>

The experimental studies on cell transplantation into chronic ischemic myocardium using mesenchymal stem cells modified by recombinant adenovirus carrying vascular endothelial growth factors 165 gene / 中华外科杂志

<p><b>OBJECTIVE</b>To observe the therapeutic effect of vascular endothelial growth factors 165 (VEGF165) gene expressing mesenchymal stem cells (MSCs) in chronic myocardial infarction model by providing enhanced cardioprotection, followed by angiogenic effects in infarcted myocardium.</p><p><b>METHODS</b>Recombinant adenovirus vector carrying VEGF165 gene (rAd-VFGF165) was constructed. MSCs were harvested through gradient centrifugation, then were cultivated, multiplied and expanded. Recombinant adenoviruses mediated VEGF165 gene were transfected into MSCs, and the MSCs were labelled by DAPI. The left anterior descending branch of rabbits were ligated to establish a myocardial infarction model; and the animals survived for 6 weeks were randomly divided into three groups: VEGF165-expressing MSCs transplanted (Group I), MSCs transplanted (Group II) and dulbecco modified eagles medium injected (Group III). At 4 weeks after cell transplantation, the MSCs were detected by DAPI staining in infarcted region. The cardiac functions were estimated by UCG. The microvascular density in infarcted area were estimated through CD34 immunohistochemical analysis.</p><p><b>RESULTS</b>Four weeks after cell transplantation, ejection fraction, E wave/A wave ratio and capillary density of the infarcted region were most improved in Group I compared with Group II and control group (P < 0.05). DAPI positive cells were most increased in Group I.</p><p><b>CONCLUSIONS</b>The transplantation of VEGF165-expressing MSCs had a better therapeutic effect than the transplantation of simplex MSCs. This combined strategy of MSCs transplantation with vgene therapy could be a useful therapy for the treatment of myocardial infarction.</p>