Newton G E, Parker J D
Department of Medicine, Mount Sinai Hospital, University of Toronto, Ontario, Canada.
Circulation. 1996 Dec 15;94(12):3161-7. doi: 10.1161/01.cir.94.12.3161.
Although there is indirect evidence of impaired baroreflex control of sympathetic outflow directed at heart muscle, the regulation of cardiac sympathetic activity in the setting of heart failure is largely unexplored. We used the norepinephrine spillover method to address the hypothesis that baroreflex control of cardiac sympathetic activity is reduced in heart failure.
Twenty-three patients were studied, 17 in a group with heart failure and 6 in a group with normal ventricular function. In both groups, cardiac norepinephrine spillover was assessed in response to nitroprusside infused to steady-state conditions. Nitroprusside resulted in significant reductions in mean systemic arterial pressure (normal group, -15 +/- 3% [mean +/- SEM]; heart failure group, -13 +/- 1%) and mean pulmonary artery pressure (normal group, -25 +/- 10%; heart failure group, -29 +/- 4%). In response to nitroprusside, there was a 98 +/- 16% increase in cardiac norepinephrine spillover in the normal group (from 81 +/- 10 to 159 +/- 25 pmol/min, P < .05). Despite similar hemodynamic responses to nitroprusside in the heart failure group, there was only a 28 +/- 14% increase in cardiac spillover (from 211 +/- 71 to 245 +/- 59 pmol/ min, P = NS), a response that was significantly smaller than that seen in the normal group.
In patients with heart failure compared with subjects with normal ventricular function, there was a significantly smaller increase in cardiac sympathetic activity in response to a steady-state infusion of nitroprusside. This result provides evidence for reduced baroreflex control of cardiac sympathetic activity in heart failure.
尽管有间接证据表明针对心肌的压力反射对交感神经流出的控制受损，但心力衰竭时心脏交感神经活动的调节在很大程度上仍未被探索。我们使用去甲肾上腺素溢出方法来验证心力衰竭时心脏交感神经活动的压力反射控制减弱这一假说。
研究了23例患者，其中17例为心力衰竭组，6例为心室功能正常组。在两组中，均在硝普钠输注至稳态条件下评估心脏去甲肾上腺素溢出情况。硝普钠导致平均体循环动脉压显著降低（正常组，-15±3%[平均值±标准误]；心力衰竭组，-13±1%）和平均肺动脉压显著降低（正常组，-25±10%；心力衰竭组，-29±4%）。在正常组中，对硝普钠的反应是心脏去甲肾上腺素溢出增加98±16%（从81±10增至159±25 pmol/min，P<.05）。尽管心力衰竭组对硝普钠的血流动力学反应相似，但心脏溢出仅增加28±14%（从211±71增至245±59 pmol/min，P=无统计学意义），该反应明显小于正常组。
与心室功能正常的受试者相比，心力衰竭患者在稳态输注硝普钠时心脏交感神经活动的增加明显较小。这一结果为心力衰竭时心脏交感神经活动的压力反射控制减弱提供了证据。
