AIM:To investigate the effect of short-chain acyl-CoA dehydrogenase ( SCAD) on collagen expres-sion and proliferation of rat cardiac fibroblasts and to explore the relationship between SCAD and cardiac fibrosis . METHODS:The model of proliferation and collagen expression of rat cardiac fibroblasts induced by angiotensin II was es -tablished.After treatment with siRNA-1186, the expression of SCAD at mRNA and protein levels , fatty acids beta oxida-tion rate, ATP, the enzyme activity of SCAD and free fatty acids in the rat cardiac fibroblasts were determined . RESULTS:The mRNA and protein expression of SCAD was decreased in the rat cardiac fibroblasts induced by angiotensin II compared with the control cells , and the expression of collagen I and collagen III was significantly upregulated .Com-pared with negative control group , SCAD expression and activity , fatty acid beta-oxidation rate and ATP significantly de-creased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the rat cardiac fibroblasts , and the expression of collagen I and collagen III was significantly up-regulated.CONCLUSION:The expression and synthesis disorder of collagen may be triggered by down-regulation of SCAD .SCAD may be a promising therapeutic target for myocar-dial fibrosis .

Objective To investigate the effects of intravenous infusion of methoxamine and phenylephrine on blood pressure and coronary artery blood flow in elderly patients with post volume treatment hypotension after cardiopulmonary bypass (CPB ) undergoing coronary artery bypass grafting (CABG).Methods Forty patients,physical status ASA Ⅱ or Ⅲ,>65 years old,undergo-ing CABG,following CPB,with a mean arterial pressure (MAP)<70% of baseline,despite adequate volume replacement (based on achieving a normal CVP),were randomly assigned to me-thoxamine group (group M,n=20)or phenylephrine group (group P,n=20).The initial infusion rate was 3 μg·kg-1·min-1in group M and 0.24 μg·kg-1·min-1in group P,respectively.The rate was increased or decreased by one third of initial dose in order to maintain the MAP at the target level (±20% of baseline MAP).Coronary sinus (CS),systolic blood flow velocity time integral (SV-TI),diastolic velocity time integral (DVTI),CS blood flow (CSBF)were recorded before adminis-tration,at 3,5,10,15,30 min after administration.Results Compared with pre-administration,SV-TI,DVTI,CSBF were increased at each point in the two groups (P<0.05 or P<0.01).SVI was in-creased at 15 min and 30 min in group M (P<0.05).Compared with group P,DVTI and CSBF at 10,15 min and 30 min was higher in group M (P<0.05 or P<0.01).There were 2 cases of atrial fibrillation and 1 case of frequent ventricular premature beat after operation in group M;1 case of bradycardia and 1 case of frequent ventricular premature beats after operation in group P.Conclusion Intravenous infusion of methox-amine and phenylephrine both can correct post volume treatment hypotension after CPB in elderly patients undergoing CABG,but methoxamine increases coronary blood flow more significantly and may be more ben-eficial to patients with coronary heart disease.

Objective To observe the changes of short-chain acyl-CoA dehydrogenase (SCAD) expression on human umbilical vein endothelial cell (HUVEC) apoptosis and investigate its relationship with apoptosis. Methods The HUVEC was cultured normally for 2-3 days. The apoptotic model of HUVEC was established by tert-butyl hydrogen peroxide (tBHP). The HUVEC was treated by different concentrations of tBHP (0, 10, 20, 30, 40, 50 μmol/L) for 12 hours and different time (0, 3, 6, 9, 12 hours) with 50 μmol/L tBHP to establish the apoptotic model of HUVEC. The cell viability was detected by methyl thiazolyl tetrazolium (MTT), the mRNA expression of SCAD was determined by real-time polymerase chain reaction (PCR), the protein expression of SCAD was achieved by Western Blot. The best concentrate and time were determined to interfere the HUVEC to achieve the apoptotic model of HUVEC. The SCAD gene of HUVEC was knocked down by RNA interference sequence (siRNA274, siRNA414, siRNA679). The mRNA expression of SCAD, the protein expression of SCAD and the activity of SCAD enzyme were detected to achieve the best RNA interference sequence. The HUVEC was intervened by the best RNA interference sequence and tBHP. The cell activity and apoptosis rate, the enzyme activity of SCAD, the mRNA and protein expression of SCAD, the contents of reactive oxygen species (ROS), aderosine triphosphate (ATP) and free fatty acid (FFA) were detected to observe the effect of SCAD on apoptosis of HUVEC. Results ① The cell viability, the mRNA expression and the protein expression of SCAD were decreased gradually in a concentration and time dependent manner with the increase of tBHP concentration and the prolongation of intervention time. The decline was most significant in the group of the 50 μmol/L tBHP to interfere HUVEC for 12 hours. ② The siRNA679 transfection was the most significant in reducing SCAD mRNA and protein expressions among the three interference sequences (siRNA274, siRNA414, siRNA679). ③ Compare with blank control group, the cell viability was significantly decreased in the siRNA679 group (A value: 0.48±0.09 vs. 1.00±0.09, P < 0.01), the apoptotic rate of HUVEC was significantly increased [(29.96±2.09)% vs. (2.90±1.90)%, P < 0.01], the expression of SCAD mRNA and SCAD protein, the activity of SCAD enzyme and the content of ATP were significantly decreased [SCAD mRNA (2-ΔΔCt): 0.50±0.16 vs. 1.34±0.12, SCAD/α-Tubulin: 0.67±0.11 vs. 1.00±0.06, the activity of SCAD enzyme (kU/g): 0.38±0.04 vs. 0.53±0.04, the content of ATP (μmol/g): 0.14±0.02 vs. 0.19±0.01, all P < 0.05], the contents of FFA and ROS were significantly increased [FFA (nmol/g): 0.84±0.07 vs. 0.47±0.04, ROS (average fluorescence intensity): 647.5±23.7 vs. 434.2±46.5, both P < 0.01]. Meanwhile, SCAD siRNA treatment triggered the same apoptosis as HUVEC treated with tBHP. Conclusions Down-regulation of SCAD may play an important role in HUVEC apoptosis. Increase in the expression of SCAD may become an important part in intervening HUVEC apoptosis.

Objective? To?Study?the?changes?of?short-chain?acyl-CoA?dehydrogenase?(SCAD)?in?heart?failure?(HF)?after?myocardial?infarction?(MI),?and?the?effect?of?aerobic?exercise?on?SCAD.? Methods? Healthy?male?Sprague-Dawley?(SD)?rats?were?divided?into?sham?operation?group?(Sham?group),?sham?operation?swimming?group?(Sham+swim?group),?HF?model?group?(LAD?group)?and?HF?swimming?group?(LAD+swim?group)?by?random?number?table?method,?with?9?rats?in?each?group.?The?left?anterior?descending?branch?of?coronary?artery?(LAD)?was?ligated?to?establish?a?rat?model?of?HF?after?MI.?In?Sham?group,?only?one?loose?knot?was?threaded?under?the?left?coronary?artery,?and?the?rest?operations?were?the?same?as?those?in?LAD?group.?Rats?in?Sham+swim?group?and?LAD+swim?group?were?given?swimming?test?for?1?week?after?operation?(from?15?minutes?on?the?1st?day?to?60?minutes?on?the?5th?day).?Then?they?were?given?swimming?endurance?training?(from?the?2nd?week?onwards,?60?minutes?daily,?6?times?weekly,?10?weeks?in?a?row).?Tail?artery?systolic?pressure??(SBP)?was?measured?before?swimming?endurance?training?and?every?2?weeks?until?the?end?of?the?10th?week.?Ten?weeks?after?swimming?training,?echocardiography?was?performed?to?measure?cardiac?output?(CO),?stroke?volume?(SV),?left?ventricular?ejection?fraction?(LVEF),?shortening?fraction?(FS),?left?ventricular?end-systolic?diameter?(LVESD),?left?ventricular?end-diastolic?diameter?(LVEDD),?left?ventricular?end-systolic?volume?(LVESV),?and?left?ventricular?end-diastolic??volume?(LVEDV).?Morphological?changes?of?heart?were?observed?by?Masson?staining.?Apoptosis?of?myocardial?cells?was?detected?by?transferase-mediated?deoxyuridine?triphosphate-biotin?nick?end?labeling?stain?(TUNEL)?and?apoptosis?index?(AI)?was?calculated.?Reverse?transcription-polymerase?chain?reaction?(RT-PCR)?and?Western?Blot?were?used?to?detect?the?mRNA?and?protein?expression?of?myocardial?SCAD?respectively.?In?addition,?the?enzyme?activity?of?SCAD,?the?content?of?adenosine?triphosphate?(ATP)?and?free?fatty?acid?(FFA)?in?serum?and?myocardium?were?detected?according?to?the?kit?instruction?steps.? Results? Compared?with?Sham?group,?Sham+swim?group?showed?SBP?did?not?change?significantly,?with?obvious?eccentric?hypertrophy?and?increased?myocardial?contractility,?and?LAD?group?showed?persistent?hypotension,?obvious?MI,?thinning?of?left?ventricle,?and?decreased?myocardial?systolic/diastolic?function.?Compared?with?LAD?group,?SBP,?systolic/diastolic?function?and?MI?in?LAD+swim?group?were?significantly?improved?[SBP?(mmHg,?1?mmHg?=?0.133?kPa):?119.5±4.4?vs.?113.2±4.5?at?4?weeks,?120.3±4.0?vs.?106.5±3.7?at??6?weeks,?117.4±1.3?vs.?111.0±2.3?at?8?weeks,?126.1±1.6?vs.?119.4±1.9?at?10?weeks;?CO?(mL/min):?59.10±6.31?vs.?33.19±4.76,?SV?(μL):?139.42±17.32?vs.?84.02±14.26,?LVEF:?0.523±0.039?vs.?0.309±0.011,?FS:?(28.17±2.57)%?vs.?(15.93±3.64)%,?LVEDD?(mm):?8.80±0.19?vs.?9.35±0.30,?LVESD?(mm):?5.90±0.77?vs.?7.97±0.60,?LVEDV?(μL):?426.57±20.84?vs.?476.24±25.18,?LVESV?(μL):?209.50±25.18?vs.?318.60±16.10;?AI:?(20.4±1.4)%?vs.?(31.2±4.6)%;?all?P??0.05).? Conclusion? The?expression?of?SCAD?in?HF?was?significantly?down-regulated,?and?the?expression?was?significantly?up-regulated?after?aerobic?exercise?intervention,?indicating?that?swimming?may?improve?the?severity?of?HF?by?up-regulating?the?expression?of?SCAD.