Diedrich André, Jordan Jens, Tank Jens, Shannon John R, Robertson Rosemarie, Luft Friedrich C, Robertson David, Biaggioni Italo
Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN 37232-2195, USA.
J Hypertens. 2003 Sep;21(9):1677-86. doi: 10.1097/00004872-200309000-00017.
To determine if the contribution of the sympathetic nervous system to blood pressure could be evidenced by low-frequency oscillations of systolic blood pressure (LF(SBP)), reflecting vascular sympathetic modulation, or by the decrease in blood pressure after autonomic blockade.
We studied multiple system atrophy (MSA) patients, in whom supine hypertension is maintained by residual sympathetic tone ('positive controls'); pure autonomic failure (PAF) patients, in whom supine hypertension is largely independent of sympathetic tone ('negative controls'); essential hypertensive patients (HTN) and normotensive subjects (NTN).
Supine systolic blood pressure (SBP) was 204 +/- 8, 185 +/- 6, 177 +/- 9 and 130 +/- 4 mmHg in MSA, PAF, HTN and NTN, respectively. LF(SBP) was higher in MSA and HTN (5.7 +/- 1.5 and 5.8 +/- 1.4 mmHg(2) compared to NTN and PAF (3.3 +/- 0.5 and 1.1 +/- 0.5 mmHg(2). Trimethaphan 2-4 mg/min induced complete autonomic blockade and lowered SBP below 125 mmHg in all NTN and all but one MSA (to 111 +/- 3 and 97 +/- 9 mmHg). SBP remained elevated in PAF (164 +/- 7 mmHg). Responses in HTN were variable; SBP decreased below 125 mmHg in three and remained elevated in four patients. The decrease in LF(SBP) correlated with the reduction in SBP, with a steeper slope in MSA and HTN compared to NTN (29.0 +/- 5.5, 8.4 +/- 1.6 and 3.6 +/- 1.2 mmHg/mmH (2), respectively).
Ganglionic blockade, alone or coupled to LF(SBP), discriminated between human models of sympathetic-dependent (MSA) and independent (PAF) hypertension. This approach may aid in assessing the contribution of the sympathetic nervous system in essential hypertension, in which sympathetic dependence is variably expressed.
确定交感神经系统对血压的影响能否通过反映血管交感神经调节的收缩压低频振荡(LF(SBP)),或自主神经阻滞后血压的下降来证实。
我们研究了多系统萎缩(MSA)患者(“阳性对照”,其仰卧位高血压由残余交感神经张力维持)、纯自主神经功能衰竭(PAF)患者(“阴性对照”,其仰卧位高血压在很大程度上与交感神经张力无关)、原发性高血压患者(HTN)和血压正常受试者(NTN)。
MSA、PAF、HTN和NTN患者的仰卧位收缩压(SBP)分别为204±8、185±6、177±9和130±4 mmHg。MSA和HTN患者的LF(SBP)高于NTN和PAF患者(分别为5.7±1.5和5.8±1.4 mmHg²,而NTN和PAF患者为3.3±0.5和1.1±0.5 mmHg²)。三甲噻方2 - 4 mg/min诱导完全自主神经阻滞,并使所有NTN患者以及除1例以外的所有MSA患者的SBP降至125 mmHg以下(分别降至111±3和97±9 mmHg)。PAF患者的SBP仍升高(164±7 mmHg)。HTN患者的反应各不相同;3例患者的SBP降至125 mmHg以下,4例患者的SBP仍升高。LF(SBP)的下降与SBP的降低相关,与NTN相比,MSA和HTN患者的斜率更陡(分别为29.0±5.5、8.4±1.6和3.6±1.2 mmHg/mmH²)。
神经节阻滞单独或与LF(SBP)结合,可区分交感神经依赖性(MSA)和非依赖性(PAF)高血压的人体模型。这种方法可能有助于评估交感神经系统在原发性高血压中的作用,在原发性高血压中交感神经依赖性表现各异。