The effect of oxygen stress on endothelin-1 in heart failure rats and the interferences of β-blockers
LI Faq
Abstract
LI Faq
Abstract
Objectives To investigate the effect of oxygen stress on the expression of cardiac endothelin 1 in chronic congestive heart failure rats, and to compare the differences between the third generation blocker, carvedilol, and the second one atenolol. Methods 8 weeks after partially banding abdominal aortic artery, 30 wistar rats were randomly divided into three groups: ①Heart group ( n= 10); ②Atenolol group ( n= 10); ③Carvedilol group ( n= 10). Meanwhile, sham operated rats ( n= 10) was established as a control group. After 4 weeks of remedy, hemodyna mic parameters, ventricular mass index (LVMI and RVMI), oxygen stress including superoxide dismutase (SOD) and malondialdehyde (MDA), and myocardiac endothelin 1 expression were studied. Results Compared with sham operated rats, all the hemodynamics were deteriorated, and LVMI and RVMI were increased significantly. Plasma MDA was on rise while SOD decreased, and cardiac endothelin 1 gene was over expressed in heart failure group ( P 0 001,0 01). LVMI was positively related to the expression of endothelin 1 gene, r =0 672 ( P 0 05). In addition, the expression of endothelin 1 was positively associated with plasma MDA but negatively with SOD activity, r= 0 836, -0.744 , respectively ( P 0 01,0 02). After carvedilol therapy, LVMI and RVMI were declined and SOD and MDA were improved in carvedilol group ( P 0 01,0 05). Moreover, myocardiac endothelin 1 gene was down expressed ( P 0 01). However, no significant change was seen in atenolol group ( P 0 05), except for only a few hemodynamic parameters. Conclusions Oxygen stress may influence the expression of cardiac endothelin 1, and endothelin 1 takes part in ventricular remodeling. Carvedilol can improve ventricular remodeling, whose mechanism may be its inhibition of oxygen stress and improvement of endothelin 1 over expression. In comparison with the same dosage of atenolol, carvedilol is more beneficial for prognosis of heart failure.
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Objectives To investigate the effect of oxygen stress on the expression of cardiac endothelin 1 in chronic congestive heart failure rats, and to compare the differences between the third generation blocker, carvedilol, and the second one atenolol. Methods 8 weeks after partially banding abdominal aortic artery, 30 wistar rats were randomly divided into three groups: ①Heart group ( n= 10); ②Atenolol group ( n= 10); ③Carvedilol group ( n= 10). Meanwhile, sham operated rats ( n= 10) was established as a control group. After 4 weeks of remedy, hemodyna mic parameters, ventricular mass index (LVMI and RVMI), oxygen stress including superoxide dismutase (SOD) and malondialdehyde (MDA), and myocardiac endothelin 1 expression were studied. Results Compared with sham operated rats, all the hemodynamics were deteriorated, and LVMI and RVMI were increased significantly. Plasma MDA was on rise while SOD decreased, and cardiac endothelin 1 gene was over expressed in heart failure group ( P 0 001,0 01). LVMI was positively related to the expression of endothelin 1 gene, r =0 672 ( P 0 05). In addition, the expression of endothelin 1 was positively associated with plasma MDA but negatively with SOD activity, r= 0 836, -0.744 , respectively ( P 0 01,0 02). After carvedilol therapy, LVMI and RVMI were declined and SOD and MDA were improved in carvedilol group ( P 0 01,0 05). Moreover, myocardiac endothelin 1 gene was down expressed ( P 0 01). However, no significant change was seen in atenolol group ( P 0 05), except for only a few hemodynamic parameters. Conclusions Oxygen stress may influence the expression of cardiac endothelin 1, and endothelin 1 takes part in ventricular remodeling. Carvedilol can improve ventricular remodeling, whose mechanism may be its inhibition of oxygen stress and improvement of endothelin 1 over expression. In comparison with the same dosage of atenolol, carvedilol is more beneficial for prognosis of heart failure.
Key concepts: Carvedilol, Atenolol, Malondialdehyde, Medicine, Internal medicine, Endothelin receptor, Heart failure, Endothelin 1