Objective To evaluate the effects of percutaneous balloon mitral valvuloplasty (PBMV) in patients with mitral stenosis (MS) and MS associated with aortic regurgitation (AR) of mild to moderate degree. Methods The results of PBMV in the Group A of 26 patient with MS associated with AR of mild to moderate degree and the group B of 34 patient with MS without AR were analyzed and compared.Results In group A, the mean left atrial pressure (MLAP) was 23.5?4.6 mm?Hg and 11.2?2.9 mm?Hg ( P

Objective To evaluate the relevance between transthoracic echocardiography(TTE)and cardiac catheterization in measuring diameter of patent ductus arteriosus(PDA)and assessing pulmonary artery pressure.Methods The diameter of PDA and the pulmonary artery pressure in 105 patients were observed by TTE and cardiac catheterization,respectively.Results The di-ameter of the narrowest segment of the ductus and pulmonary artery pressure measurements by TTE and cardiac catheterization showed excellent correlation(r=0.782,P<0.01;r=0.810,P<0.01,respectively).Conclusion TTE and cardiac catheterization for measuring diameter of PDA and pulmonary artery pressure show excellent correlation.TTE plays an important role in evaluating pulmonary artery pressure and selecting patients efficiency of PDA occlusion.

Objective To investigate the effects of calcium - dependent and calcium - independent in myosin light chain(MLC)dephosphorylation on pulmonary hemodynamics and right ventricular remodeling,and to observe whether there is a superimposition effect while intervention is conducted in two ways at the same time. Methods Ac-cording to random number table,50 rats were divided into 5 groups:sham operation group,model group,3 mg/(kg·d) ML - 7[MLC kinase(MLCK)inhibitor]treating group(M group),20 mg/(kg·d)Fasudil(Rho kinase inhibitor) treating group(F group)and 3 mg/(kg·d)ML - 7 plus 20 mg/(kg·d)Fasudil treating group(M + F group). The shunt between the abdominal aorta and inferior vena cava was used to establish rat models of pulmonary hypertension in-duced by high pulmonary flow in group of C and the experimental groups. The sham operation group was given a sham operation. MLCK and Rho kinase inhibitor were administrated intraperitoneally to rats with the shunt. After 8 weeks of shunting,mean right ventricular pressure(MRVP),mean pulmonary arterial pressure(MPAP),right ventricular hyper-trophy index(RVHI)and width of inferior venacava were evaluated by the right cardiac catheterization procedure. Results Compared with the sham operation group,MRVP,MPAP,and RVHI were obviously elevated in the model group [(2. 65 ±0. 57)kPa vs(4. 19 ±0. 67)kPa;(2. 42 ± 0. 48)kPa vs(4. 04 ± 0. 61)kPa,F = 295. 368,263. 912,all P ﹤0. 01;(0. 21 ±0. 01)g/ g vs(0. 41 ±0. 03)g/ g,F =247. 024,P ﹤0. 01]. Compared with model group,the MRVP,MPAP and RVHI in M group and F group were decreased significantly[(3. 51 ± 0. 47)kPa vs(4. 19 ± 0. 67)kPa;(3. 68 ± 0. 55)kPa vs(4. 19 ±0. 67)kPa,all P ﹤0. 01;M group:(0. 29 ±0. 02)g/ g,model group:(0. 41 ± 0. 03)g/ g,F group (0. 30 ±0. 03)g/ g,F =247. 024,P ﹤0. 05]. But the MRVP,MPAP and RVHI in M group and F group were higher than those of rats in the sham operation group. The MRVP,MPAP and RVHI of M + F group were elevated much obviously compared with those of the M or F group(P ﹤0. 05). Conclusions The calcium - dependent and calcium - independent in MLC dephosphorylation can respectively restrain the development of pulmonary hypertension and right ventricular re-modeling,and the obvious additive effect can be observed when the 2 drugs are used jointly.

[ ABSTRACT] AIM:To investigate the changes of peroxisome proliferator-activated receptors ( PPAR)α/peroxi-some proliferator activated receptor coactivator 1 alpha ( PGC-1α) in doxorubicin ( DOX) induced dilated cardiomyopathy ( DCM) and its effect on the energy metabolism and myocardial function in mice .METHODS:Forty mice were randomly divided into 4 groups:control group, DOX group, PPARαinhibitor group and PPARαagonist group.The DCM model was established by injection of DOX.The protein levels of PPARα/PGC-1αwere detected.The PPARαinhibitor and PPARαagonist were used 2 weeks beforeinjection of DOX.The contents of adenine acid and phosphocreatine ( Pcr) in the mito-chondria were measured by high-performance liquid chromatography ( HPLC) .The ANT activity was analyzed by the atrac-tyloside-inhibitor stop technique.The changes of the echocardiography and hemodynamics were also observed.RESULTS:DOX induced DCM model was successfully established.The protein levels of PPARαand PGC-1αin control group were significantly higher than those in DOX group (P<0.05).Both of the high-energy phosphate contents and the transport ac-tivity of ANT were decreased in DOX group (P<0.05), and the hemodynamic parameters were disordered (P<0.01). Compared with DOX group, PPARαinhibitor pre-treatment significantly reduced the PPARα/PGC-1αexpression.Mean-while, high-energy phosphate contents in the mitochondria and the ANT transport activity of the mitochondria decreased, as well as the left ventricular function ( P<0.05) .On the other hand, PPARαagonist significantly increased the expression of PPARαand PGC-1α, and improved the transport activity of ANT.In addition, the hemodynamic parameters were amel-iorated, but the high-energy phosphate contents of the mitochondria did not significantly change.CONCLUSION:PPARα/PGC-1αplays an important role in the regulation of ANT transport activity in dilated cardiomyopathy induced by DOX, and the activation of PPARα/PGC-1αhas protective effects on the DCM induced by DOX.

OBJECTIVE: To investigate the geometric changes and ventricular function of heart after percutaneous closure of atrial septal defect according to patient age at the time of the procedure. METHODS: A total of 109 patients with atrial septal defect admitted to Department of Cardiology, Guizhou Provincial People's Hospital between June 1998 and October 2008 were retrospectively analyzed, including 53 males and 56 females aged 3.5-70 years. According to their age, the patients were divided into child group (aged=7 years, n=31), adolescent group (n=42, aged 8 18years) and adult group (n=36, aged > 18 years). Cardiac remodeling was assessed by transthoracic echocardiography before ASD closure and 6 months after atrial septal defect closure, including lateral diameter of left and right atrium (LALD, RALD), ratio of LALD/RALD, diastolic diameter of left and right ventricle (LVDD, RVDD), RVDD/LVDD ratio, and pulmonary diameter (PD), ejection fraction (EF) of LV and RV. RESULTS: 109 patients were all included in final analysis. Compared with preoperative results, the right atrium, RALD, RVDD,RALD/LALD, RVDD/LVDD ratio and PD were significantly decreased, while the left atrium and LALD significantly increased,and EF of left and right atrium was remarkably improved 6 months following atrial septal defect closure (P< 0.05-0.01).Moreover, the heart remodeling and heart function amelioration after atrial septal defect closure of child group were better than adolescent and adult groups (P < 0.05), but there were no significant differences between adolescent and adult groups (P>0.05).CONCLUSION: Transcatheter closure of atrial septal defect is safe and effective for all patients of different ages; in particular,results at children stage are better than adolescent and adult stages.

Twenty-seven cases of simple type 2 diabetes mellitus,30 cases of coronary heart disease,and 32 cases of type 2 diabetes with coronary heart disease were enrolled in this study according to the results of coronary angiography.Meanwhile,32 healthy subjects were taken as a control group.The serum matrix metalloproteinase-9 (MMP-9) and other clinical and laboratory parameters were determined.The results showed that serum MMP-9 may play a minor role in the progression of coronary heart disease in type 2 diabetic patients.

[ABSTRACT]AIM:Toinvestigatetheeffectsofmechanicalstretchontransientoutwardpotassiumcurrent(Ito), inward rectifier potassium current ( IK1 ) and action potential duration ( APD) of cultured neonatal rat atrial myocytes . METHODS:Neonatal rat atrial myocytes were isolated and cultured on silicone sheeting with or without stretch for 24 h. The silicone membrane area was increased by 12%in stretched group.The cells without stretch served as control .Ito, IK1 and APD were recorded by the technique of whole-cell patch clamp.RESULTS:Compared with control group, Ito density in stretched myocytes was significantly reduced [(1.6 ±0.4) pA/pF vs (12.1 ±2.9) pA/pF, P<0.01], whereas IK1 density was increased [(-10.8 ±0.8) pA/pF vs (-8.8 ±0.9) pA/pF, P<0.01].The APDs at 50%and 90%levels of repolarization ( APD50 and APD90 ) in the stretched cells were obviously decreased than those in non-stretched cells [(10.5 ±1.4) ms vs (15.5 ±2.4) ms, (30.0 ±2.8) ms vs (56.3 ±3.6) ms, P<0.01].CONCLUSION: Stretch stimulation leads to the reduction of Ito density, the increase in IK1 density and the shortness of APD in cultured rat atrial neonatal myocytes , which may contribute to atrial electrical remodeling induced by pressure overload .

AIM: To investigate the effect of inhibiting myosin light chain kinase ( MLCK) on endothelin-1 (ET-1) induced proliferation and apoptosis of rat pulmonary artery smooth muscle cells (PASMCs).METHODS: Rat PASMCs were cultured and stimulated with ET-1.The cells were randomly divided into control group , ET-1 group and ET-1+MLCK inhibitor group (ET-1+M).Western blotting, MTT assay, [3H]-TdR incorporation and flow cytometry were employed to test the expression of myosin light chain (MLC) and MLCK, cell proliferation, cell cycle and apoptotic rate of PASMCs ,respectively .The phosphorylation of MLC was determined by glycerol-PAGE coupled with Western blotting .RE-SULTS:Compared with control group , the protein expression of MLCK and MLC phosphorylation significantly enhanced af -ter ET-1 stimulation.ET-1 markedly induced the proliferation and decreased the percentage of apoptotic rate in the PASMCs.However, pretreatment with ML-7, a MLCK inhibitor, significantly reversed the above effects induced by ET-1. CONCLUSION:MLCK inhibitor effectively inhibits the ET-1-induced proliferation and the cell cycle progression .

AIM:To study the effects and mechanism of peroxisome proliferator-activated receptors(PPARs)ligands,fenofibrate and pioglitazone,on ventricular remodeling in pressure overload rats.METHODS:A pressure overload model was established by the constriction of abdominal aorta in Wistar rats.The hemodynamics and ventricular remodeling parameters,plasma and myocardial renin activity,angiotensin Ⅱ and aldosteron,the mRNA expression of angiotensin Ⅱ type 1 receptor(AT1)were investigated in the constriction of abdominal aorta group(CAA group,n=7)at 12-week after operation and treated experimental groups in which rats were treated with fenofibrate(F group,n=8),pioglitazone(P group,n=7),concomitant fenofibrate and pioglitazone(F+P group,n=6)for 12 weeks since 2 days after operation.The sham-operated rats served as controls(n=8).RESULTS:The ratio of left ventricular weight to body weight,mean arterial pressure,left ventricular systolic pressure,left ventricular end diastolic pressure,left ventricular systolic pressure and heart rate were significantly lower,the maximum left ventricular pressure rising and declining rates(?dp/dtmax)were significantly higher in all treated experimental groups than those in CAA group.Fenofibrate or pioglitazone had no effect on plasma and myocardial levels of renin,angiotensin Ⅱand aldosteron.The mRNA expression of AT1 was downregulated in treated groups except F group.CONCLUSION:PPAR ligands have no effect on plasma and myocardial levels of renin,angiotensin Ⅱand aldosteron,but fenofibrate and pioglitazone inhibit ventricular remodeling,decrease preload and afterload,increase ?dp/dtmax in pressure overload rats.The expression of mRNA of AT1 is downregulated in myocardium of pressure overload rats by the PPAR? signaling pathway.

OBJECTIVETo explore the effect of Schlafen 1 (Slfn1) on the migration of endothelial progenitor cells (EPCs).

METHODSRat bone marrow derived EPCs were isolated and cultured. Ad-Slfn1, ShRNA-Slfn1, ShRNA-control and Ad-control were transfected into EPCs respectively. The mRNA expression of Slfn1 and Cyclin D1 was examined by reverse transcriptase-PCR, and their protein expression was detected by Western blot. The migration of EPCs was examined by a modified Boyden chamber assay.EPCs cell cycle was determined using flow cytometry analysis.

RESULTSForty-eight hours after ShRNA-Slfn1 transfection, the mRNA and protein expression of Slfn1 in EPCs was significantly down-regulated compared to ShRNA-control EPCs (P < 0.05). Transfection of Ad-Slfn1 reversed these changes.Overexpression of Slfn1 reduced the migration capacity of EPCs while the silencing of Slfn1 by shRNA-Slfn1 increased the migration capacity of EPCs.In addition, cell cycle was arrested at G1 phase in Slfn1 overexpression group while transfection of shRNA-Slfn1 reversed these responses.Interestingly, the mRNA and protein expression of Cyclin D1 was significantly up-regulated after shRNA-Slfn1 transfection compared to ShRNA-control group (all P < 0.05), but overexpression of Slfn1 reversed these results, suggesting Cyclin D1 was involved in regulating EPCs cell cycle via Slfn1 signaling.

CONCLUSIONSSlfn1 could reduce the migration capacity of EPCs via Cyclin D1 pathway.

Animals ; Cell Cycle ; Cell Cycle Proteins ; physiology ; Cell Division ; Cell Movement ; Cyclin D1 ; physiology ; Down-Regulation ; Endothelial Progenitor Cells ; Flow Cytometry ; In Vitro Techniques ; RNA, Messenger ; RNA, Small Interfering ; Rats ; Transfection ; Up-Regulation