Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan; Department of Laboratory Medicine, Nagoya University Hospital, Nagoya, Japan.
Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Parkinsonism Relat Disord. 2014 Apr;20(4):409-14. doi: 10.1016/j.parkreldis.2014.01.003. Epub 2014 Jan 14.
Cardiac sympathetic denervation is associated with orthostatic hypotension (OH) in Parkinson's disease (PD); however, the physiological role of cardiac sympathetic nerves has yet to be elucidated. To clarify the role of the heart in orthostatic stress, we evaluated whether cardiac sympathetic nerves can alter cardiac activity and systolic blood pressure (BP) in association with elevations or depressions of total peripheral resistance during the head-up tilt test.
Ninety-five PD patients and 17 normal controls were enrolled. Using impedance cardiography, we measured total peripheral resistance, stroke volume, heart rate, and systolic BP during the head-up tilt test. Cardiac denervation was defined as a heart-to-mediastinum ratio <1.7 for cardiac (123)I-metaiodobenzylguanidine uptake on delayed images.
At 60° tilt, total peripheral resistance decreased from the initial value in 49 PD patients. Among these, 36 patients exhibited cardiac denervation with severe reductions in systolic BP but little change in stroke volume; among these patients 22 had OH. The remaining 13 patients without cardiac denervation exhibited significant increases in stroke volume and well-preserved systolic BP with no OH. On the other hand, 46 patients had elevations in total peripheral resistance and reduced stroke volume, but little change in systolic BP, regardless of the presence or absence of cardiac denervation. Only one of these patients experienced OH.
Under orthostatic stress, cardiac sympathetic denervation with failure to increase total peripheral resistance leads to large reductions in systolic BP. However, patients without cardiac denervation exhibited a positive inotropic response against vasodilatation, which may prevent OH.
心脏交感神经去神经支配与帕金森病(PD)的直立性低血压(OH)有关;然而,心脏交感神经的生理作用仍有待阐明。为了阐明心脏在直立性应激中的作用,我们评估了心脏交感神经是否可以在头高位倾斜试验期间随着总外周阻力的升高或降低而改变心脏活动和收缩压(BP)。
纳入 95 例 PD 患者和 17 例正常对照者。使用阻抗心动图,我们在头高位倾斜试验期间测量了总外周阻力、每搏量、心率和收缩压。心脏去神经支配定义为延迟图像上心脏与纵隔的比值<1.7,用于心脏(123)I-间碘苄胍摄取。
在 60°倾斜时,49 例 PD 患者的总外周阻力从初始值下降。其中 36 例患者存在心脏去神经支配,收缩压显著降低,但每搏量变化不大;其中 22 例患者出现 OH。其余 13 例无心脏去神经支配的患者表现为每搏量显著增加和收缩压良好保持,无 OH。另一方面,46 例患者总外周阻力升高,每搏量减少,但收缩压变化不大,无论是否存在心脏去神经支配。这些患者中只有 1 例发生 OH。
在直立性应激下,心脏交感神经去神经支配伴总外周阻力增加不足会导致收缩压大幅降低。然而,无心脏去神经支配的患者表现出对血管扩张的正性变力反应,这可能预防 OH。