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本研究旨在通过给予去卵巢大鼠异丙肾上腺素制作心肌损伤及心功能异常模型,探讨雌激素通过调节兴奋性G(Gαs)蛋白-环磷酸腺苷(cAMP)信号通路纠正儿茶酚胺导致的心功能异常的机制。观察雌激素对大鼠血流动力学参数:左心室收缩峰压(LVSP)、左心室舒张末压(LVEDP)、左心室内压上升的最大变化速率(+dp/dtmax)、左心室内压下降的最大变化速率(-dp/dtmax),血浆脑尿钠肽(brain natriuretic peptide,BNP),cAMP浓度和心肌中Gαs蛋白表达的影响。结果显示:与假手术组相比,去卵巢大鼠的血流动力学参数、血浆BNP水平、血浆cAMP水平没有显著改变;但给予去卵巢大鼠异丙肾上腺素后,血流动力学参数LVSP、+dp/dtmax降低(P<0.01),LVEDP、-dp/dtmax升高(P<0.01),血浆BNP水平升高(P<0.01),血浆cAMP水平降低(P<0.01);而进一步的雌激素补充则改善了心功能:LVSP、+dp/dtmax升高(P<0.01),LVEDP、-dp/dtmax降低(P<0.05,P<0.01),血浆BNP水平降低(P<0.01),cAMP水平升高(P<0.01);雌激素对Gαs蛋白表达没有显著影响。结果提示:雌激素对心肌损伤具有保护作用,升高cAMP水平,改善心肌收缩过度抑制,调节心脏的功能状态。
The aim of this study was to evaluate the effects of estrogen on the regulation of catecholamines by modulating the excitatory G(Gαs) protein-cAMP signalling pathway by administering isoproterenol in ovariectomized rats. Mechanism of abnormal function. Observe the hemodynamic parameters of estrogen in rats: left ventricular systolic peak pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximum rate of left intraventricular pressure elevation (+dp/dtmax), left ventricular pressure The maximum rate of decline (-dp/dtmax), plasma brain natriuretic peptide (BNP), cAMP concentration, and expression of Gαs protein in the myocardium. The results showed that compared with the sham group, the hemodynamic parameters, plasma BNP levels, and plasma cAMP levels did not change significantly in ovariectomized rats; however, after administration of isoproterenol in ovariectomized rats, the hemodynamic parameter LVSP , +dp/dtmax decreased (P <0.01), LVEDP, -dp/dtmax increased (P <0.01), plasma BNP levels increased (P <0.01), plasma cAMP levels decreased (P <0.01); and further Estrogen supplementation improved cardiac function: LVSP, +dp/dtmax increased (P<0.01), LVEDP, -dp/dtmax decreased (P<0.05, P<0.01), and plasma BNP levels decreased (P<0.01). The level of cAMP increased (P<0.01); estrogen had no significant effect on the expression of Gαs protein. The results suggest that estrogen has a protective effect on myocardial injury, increase cAMP levels, improve myocardial contraction inhibition, and regulate cardiac function.