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Objective To investigate the relationship between the oxidized low-density lipoprotein(ox-LDL) in the blood from the coronary sinus and impaired endothelium-dependent vasodilation in patients with coronary artery disease(CHD).Methods Four groups of patients were subjected,including acute myocardial infarction group(AMI,n=22),unstable angina group(UA,n=29),and stable angina group(SA, n=25) and control group(n=20) who was first suspected as CHD and then verified with normal coronary angiograms.Blood form the coronary sinus was collected through cardiac cathetering and the ox-LDL level was measured by Sandwich ELISA method.Brachial arterial hyperemia-induced flow mediated dilation(FMD) and sublingual nitroglycerin(NTG) mediated vasodilation were measured by high resolution ultrasound.Results The blood level of ox-LDL in patients with CHD was markedly higher than those in control group(P
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Objective To study the reversion of the metabolic gene expression pattern of hypertrophic cardiac and role of Carvedilol and to explore the molecular regulatory mechanism of Carvedilol on attenuating the reversion back towards fetal energy metabolism occurring with the development of cardiac hypertrophy. Methods A model of hypertrophy induced by coarctation of abdominal aorta(CAA) in male Wistar rats was employed and changes of parameters such as hemodynamics, ventricular remodeling parameters, free fatty acid in blood serum and cardiac myocyte and expressions of muscle carnitine palmitoyltransferase Ⅰ (M CPT Ⅰ) and medium chain acyl CoA dehydrogenase (MCAD) mRNA were investigated in the experimental animals in operation group(CAA), sham operation group(SH) and Carvedilol intervention group(CAR) at 16 weeks after operation. Results Significant hypertrophy was found in the left ventricle in CAA group(3.41?1.30 vs 2.46?1.31, P
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Objective To study the mechanism of carvedilol therapy of congestive heart failure. Methods After chronic heart failure model was established by ligation of the left coronary artery in rats, rats were treated with carvedilol and terazosin. Then hemodynamic parameters, activity of sarcoplasmic reticulum(SR) Ca 2+ pump(SERCA 2a ) and the rate of cardiomyocyte apoptosis were determined. Results Compared with those of the control group( group C), the activity of SR Ca 2+ pump in the heart failure group(group F) decreased( P 0.05). Carvedilol intervention reduced the rate of cardiomyocyte apoptosis, but enhanced the activity of SR Ca 2+ pump significantly in dose dependent manner. The activity of SR Ca 2+ pump was negatively correlated with the rate of cardiomyocyte apoptosis( r =-0.814, P
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Objective To study the effects of ACE1 on amount and mRNA expression of Ca2+ release channels(RyR2) of myocardial sarcoplasmic reticulum(SR) in prevention and treatment of chronic heart failure.Methods After the model of chronic heart failure was established with ligation of left corongary artery in rats,the animals were prevented and treated with Perindopril. Hemodynamic parameters, Bmax and Kd of ［3H］－ryanodine binding to RyR2、RyR2 mRNA content were determined.Results Compared with the control group(group C),LVEDP in the heart faliure group (group F)increased(P0.05).Conclusion The amount and mRNA expression of RyR2 of myocardial sarcoplasmic reticulum(SR) decreased in chronic heart failure.Perindopril can improve mRNA expression and amount of RyR2 of myocardial SR in prevention and treatment of chronic heart failure, thus contributing to the improvement of myocardial function.
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Objective To evaluate the effects of recombinant human neuregulin-1? on a rat model of adriamycin-induced dilated cardiomyopathy(ADR-DCM).MethodsMatched adult male Sprague-Dawley rats were administered with 2.5 mg/kg adriamycin intravenously once a week for 10 weeks to establish models of ADR-DCM.The ADR-DCM rats were randomly divided into 3 groups as follows: the rhNRG-1? group(rhNRG-1?,20 ?g/kg,i.v.,once a day for 10 d,n=8),the negative control group(excipient,n=8),and the positive control group(digoxin,0.062 5 mg/kg,i.v.,once a day for 10 d,n=7).Another 8 normal SD rats in the same situation served as normal control group(control,n=8).Their heart function and hemodynamics were evaluate after the treatment.The ratio of heart weight/body weight was calculated and the thickness of LV parietes was measured.The pathological lesions of cardiac muscle tissues were evaluated after HE staining.Brain contents of natriuretic peptide(BNP) and troponin T(TnT) were determined.The animal treatment was all accorded to the ethical standards.ResultsCompare with the normal control group,the LVESD and LVEDD of ADR-DCM rats were increased(P