治疗充血性心衰的药物力药学1.ppt

心衰治疗模式的转变 长期的、修复性的策略 改变衰竭心脏的生物学特性 改善长期预后 短期血流动力学效应 Summary Pathophysiological mechanisms Neurohormonal response: sympathetic and RAAS activation Down-regulation of β1-Gs system Myocardial remodeling Cardiac glycosides Typical positive inotropic agents Inhibiting Na-K-ATPase RAAS inhibitors Neurohormonal, hemodynamics, remodeling ACEI the first line therapy of CHF AT1 blockers and spironolatone Summary Diuretics Reduce sodium and water retention Low efficacy diuretics: Counteract K+ loss β- receptor blockers Initiated with low doses Vasodilators, calcium channel blockers, untypical positive inotropic agents Not routine use for treating CHF 思考题 治疗CHF的药物有哪几类？主要代表药？ 试述强心苷正性肌力作用及作用机理 试述强心苷治疗房颤、房扑的电生理学基础？ 如何防治强心苷中毒？ 试述ACEI和β受体阻滞剂治疗心衰药理学基础？ * * Increased sympathetic outflow causes tarchycardia, increased cardiac contractility and increased vascular tone . for a relatively short time, complex Down-regulatory changes in β1-adrenoceptor-G protein-effector system take place resulting from extended activation of sympathetic system While the increased Ang2 production also lead to the increase of vascular tone, resulting in increased afterload. And ang2 can also causes aldosterone secretion leading to sodium and water retention, which may induce increase of preload. And the most harmful effect of ang2 is related to hypertrophy and remodeling of both heart and vessels. In spite of the increased force and HR and preload initially increase cardiac output, but increase of afterload and preload and cardiac hypertophy and remodeling and down-regulation of ..may result in the systolic dysfunction and diastolic dysfunction exacerbating the pathological process of CHF * 心房利钠肽(ANP)和脑利钠肽(BNP)增多 * 酮固酮拮抗药：螺内酯 * 降低衰竭心脏耗氧量 * And what is the molecular mechanisms of cardiac glycosides’s positive inotropic effects? At the molecular level, all kinds of cardiac glycosides inhibit Na/K ATPase, which is also called as the sodium pump. The protein consists of αand β subunits. The binding site f