论文部分内容阅读
Objectives To observe the effect of β3-Adrenoceptor (AR) on ventricle fibrillation threshold (VFT) and effective refractory period (ERP) in rats with heart failure. Methods Rats were randomized into control group and heart failure group. The expression of β3-ARmRNA was detected with RT-PCR; The VFT, ERP, LVESP,LVEDP, +dp/dtmax and -dp/dtmax was measured at the same time with administration of BRL37344(2 nmol/kg, β3-AR agonist). Results ①Both the expression of β3-AR mRNA and the proportion increased in rats with heart failure in comparison with control rats (0.028 vs. 0.011 and 5.4% vs 1.2%, P < 0.05); ② ERP was longer in rats with heart failure than control group (70.5±5.5 ms vs 59.5±6.4ms, P < 0.05) and there was no difference of ERP in rats with heart failure with administration of BRL37344 (73.0±4.8 ms vs 70.5±5.5 ms, P > 0.05); ③VFT was lower in rats with heart failure than control group(10.9±0.8 mv vs 30.5±1.3 mv, P < 0.05) and decreased obviously in rats with heart failure with administration of BRL37344(7.1±0.6 mv vs 10.9±0.8 mv, P < 0.05); The decrease of VFT correlated with the effect on LVESP,+dp/dtmax,-dp/dtmax of BRL37344 and the expression of β3-AR mRNA (correlation coefficient: 0.788, 0.708, 0.759, 0.787; P < 0.05). Conclusions The expre-ssion of β3-AR mRNA of left ventricle was obviously increased in rats with heart failure, and activation of β3-AR had no effect on ERP but could decreased VFT which correlated with the effect of β3-AR on LVESP, +dp/dtmax, -dp/dtmax and the expression of β3-AR mRNA.
Objectives To observe the effect of β3-Adrenoceptor (AR) on ventricle fibrillation threshold (VFT) and effective refractory period (ERP) in rats with heart failure. Methods Rats were randomized into control group and heart failure group. The expression of β3-AR mRNA was detected with RT-PCR; The VFT, ERP, LVESP, LVEDP, + dp / dtmax and -dp / dtmax was measured at the same time with administration of BRL37344 (2 nmol / kg, expression of β3-AR mRNA and the proportion increased in rats with heart failure in comparison with control rats (0.028 vs. 0.011 and 5.4% vs 1.2%, P <0.05); ② ERP was longer in rats with heart failure than control group 70.5 ± 5.5 ms vs. 59.5 ± 6.4 ms, P <0.05) and there was no difference of ERP in rats with heart failure with administration of BRL37344 (73.0 ± 4.8 ms vs. 70.5 ± 5.5 ms, P> 0.05); ③ VFT was lower in rats with heart failure than control group (10.9 ± 0.8 mv vs 30.5 ± 1.3 mv, P <0.05) and decreased obviously in rats with hear t failure with administration of BRL37344 (7.1 ± 0.6 mv vs 10.9 ± 0.8 mv, P <0.05); The decrease of VFT correlated with the effect on LVESP, + dp / dtmax, -dp / dtmax of BRL37344 and the expression of β3- AR mRNA of left ventricle was obviously increased in rats with heart failure, and activation of β3-AR had no effect (AR), correlation coefficient: 0.788, 0.708, 0.759, 0.787 on ERP but could decreased VFT which correlated with the effect of β3-AR on LVESP, + dp / dtmax, -dp / dtmax and the expression of β3-AR mRNA.