DIRECT EVIDENCE FROM INTRANEURAL RECORDINGS FOR INCREASED CENTRAL SYMPATHETIC OUTFLOW IN PATIENTS WITH HEART-FAILURE
DIRECT EVIDENCE FROM INTRANEURAL RECORDINGS FOR INCREASED CENTRAL SYMPATHETIC OUTFLOW IN PATIENTS WITH HEART-FAILURE
复制标题
DOI：
10.1161/01.cir.73.5.913
复制
发表时间：
1986-05-01
期刊：
影响因子：
37.8
通讯作者：
MARK, AL
中科院分区：
文献类型：
--
作者：
LEIMBACH, WN;WALLIN, BG;MARK, AL
心力衰竭患者有血管阻力增加和神经体液驱动增加的证据。在心力衰竭患者中可发现高水平的循环去甲肾上腺素，但尚不清楚这是否反映了交感神经活动增加，还是由于去甲肾上腺素的合成、释放或代谢改变所致。我们使用微神经摄影（腓神经）直接记录交感神经对肌肉的活动（mSNA），并测量了心力衰竭患者和正常对照者的血浆去甲肾上腺素水平。我们的目的是确定心力衰竭患者的交感神经活动是否增加，以及血浆去甲肾上腺素水平是否与心力衰竭患者的mSNA水平相关。16例中重度心力衰竭患者静息肌交感神经活动(54 .+-。5次/分钟，平均+-。（p < 0.01）显著高于9名年龄匹配的正常对照(25。4次/分钟)或19名“年轻”的正常对照对象(24 .+-。2脉冲/分钟)。我们发现血浆去甲肾上腺素水平与mSNA之间存在显著相关性（r = 0.73, p < 0.05）。mSNA和血浆去甲肾上腺素水平与全身血管总阻力、心脏指数、左心室射血分数或心率均无相关性。然而，mSNA和血浆去甲肾上腺素水平与左心室充盈压力（r = 0.80， mSNA vs充盈压力；r = 0.82，去甲肾上腺素水平vs充盈压力）和平均右心房压力呈显著正相关（p < 0.05）。该研究的结果提供了心力衰竭患者中枢交感神经流出增加的第一个直接证据，也提供了血浆去甲肾上腺素水平与这些患者的交感神经对肌肉的活动有合理关联的第一个直接证据。此外，数据表明，预负荷是这些患者SNA的重要决定因素。
Patients with heart failure have increased vascular resistance and evidence for increased neurohumoral drive. High levels of circulating norepinephrine are found in patients with heart failure, but it is not known whether they reflect increased sympathetic neural activity or result from altered synthesis, release, or metabolism of norepinephrine. We used microneurography (peroneal nerve) to directly record sympathetic nerve activity to muscle (mSNA) and also measured plasma norepinephrine levels in patients with heart failure and in normal control subjects. Our goal was to determine whether sympathetic nerve activity is increased in patients with heart failure and whether plasma norepinephrine levels correlate with levels of mSNA in heart failure. Resting muscle sympathetic nerve activity in 16 patients with moderate to servere heart failure (54 .+-. 5 bursts/min, mean .+-. SE) was significantly higher (p < .01) than the levels of activity in either nine age-matched normal control subjects (25 .+-. 4 bursts/min) or 19 "young" normal control subjects (24 .+-. 2 bursts/min). We found a signficant correlation between plasma norepinephrine levels and mSNA (r = .73, p < .05). Neither mSNA nor plasma norepinephrine levels correlated with total systemic vascular resistance, cardiac index, left ventricular ejection fraction, or heart rate. However, both mSNA and plasma norepinephrine levels showed significant positive correlations (p < .05) with left ventricular filling pressures (r = .80, mSNA vs filling pressures; r = .82, norepinephrine levels vs fillign pressures) and mean right atrial pressure. The results of the study provide the first direct evidence of increased central sympathetic nerve outflow in patients with heart faiure and the first direct evidence that plasma norepinephrine levels show a reasonable correlation with sympathetic nerve activity to muscle in these patients. Furthermore, the data suggest that preload is an important determinant of SNA in these patients.