Kubo Toshihiko, Parker John D, Azevedo Eduardo R, Atchison Deborah J, Newton Gary E, Picton Peter, Floras John S
Division of Cardiology, Mount Sinai Hospital and University Health Network Department of Medicine, University of Toronto, 600 University Avenue Suite 1614, Toronto, Ontario, Canada, M5G 1X5.
Eur J Heart Fail. 2005 Aug;7(5):878-81. doi: 10.1016/j.ejheart.2004.10.012.
We have documented a pre-junctional beta-2 adrenoceptor mediated reduction in cardiac norepinephrine spillover (CNES) in heart failure patients receiving chronic beta-blockade. Our present objective was to ascertain the consequence of this decrease for vagal heart rate (HR) regulation by determining CNES, arterial baroreflex sensitivity for HR (BRS) and arterial baroreflex modulation of muscle sympathetic nerve activity (MSNA) before and upon 4 months of beta-blockade with either carvedilol or metoprolol. In 19 heart failure patients in sinus rhythm (age: 55+/-2 [mean+/-S.E.]; ejection fraction: 20+/-2%), beta-blockade increased BRS from 4.8+/-0.9 to 7.9+/-1.3 ms/mm Hg (P<0.005) but had no effect on arterial baroreflex modulation of MSNA. Changes in CNES and BRS were inversely related (r=-0.52; n=16, P<0.05). Chronic beta-blockade in heart failure augments reflex vagal control of HR at an efferent site of interaction involving blockade of cardiac sympathetic pre-junctional beta-2 adrenoceptors that facilitate NE release.
我们已经记录到,在接受慢性β受体阻滞剂治疗的心力衰竭患者中,结前β2肾上腺素能受体介导心脏去甲肾上腺素溢出(CNES)减少。我们目前的目标是,通过在使用卡维地洛或美托洛尔进行β受体阻滞剂治疗4个月之前及之后,测定CNES、心率(HR)的动脉压力反射敏感性(BRS)以及肌肉交感神经活动(MSNA)的动脉压力反射调节,来确定这种减少对迷走神经HR调节的影响。在19例窦性心律的心力衰竭患者中(年龄:55±2[平均值±标准误];射血分数:20±2%),β受体阻滞剂治疗使BRS从4.8±0.9增加至7.9±1.3 ms/mm Hg(P<0.005),但对MSNA的动脉压力反射调节没有影响。CNES和BRS的变化呈负相关(r=-0.52;n=16,P<0.05)。心力衰竭患者的慢性β受体阻滞剂治疗在一个传出相互作用部位增强了对HR的反射性迷走神经控制,该部位涉及对促进去甲肾上腺素释放的心脏交感神经结前β2肾上腺素能受体的阻滞。