Moriguchi A, Otsuka A, Kohara K, Mikami H, Ogihara T
Department of Geriatric Medicine, Osaka University Medical School, Japan.
Am J Hypertens. 1993 Mar;6(3 Pt 1):198-203.
To evaluate the pathogenesis of orthostatic hypotension, we studied the autonomic regulation system by measuring heart rate variability during 60 degrees passive head-up tilt using power spectral analysis in 21 patients with orthostatic hypotension (mean age 62 +/- 2 years, five with histories of cerebrovascular accidents, five with Parkinsonism, five with diabetes mellitus, three with pheochromocytoma, and three with unknown causes) and 15 normal healthy subjects as a control (mean age 63 +/- 2 years). We also assessed plasma epinephrine and norepinephrine response to tilt. During tilt, control subjects showed an increase in heart rate with no change in blood pressure. Spectral analysis of heart rate variability demonstrated increases in the low frequency band (LFB, mainly sympathetic) and low frequency band/high frequency band ratio (LFB/HFB, sympatho-vagal balance). All patients with orthostatic hypotension showed a significant reduction in blood pressure with an increase in heart rate. In patients with histories of cerebrovascular accidents and with Parkinsonism, LFB and the LFB/HFB ratio did not increase. However, in other patients with orthostatic hypotension, LFB and the LFB/HFB ratio increased during tilt. Norepinephrine increased in control subjects and in patients with diabetes mellitus, pheochromocytoma, and unknown causes. In contrast, patients with histories of cerebrovascular accidents and patients with Parkinsonism showed no increase in norepinephrine. Epinephrine responses paralleled those of norepinephrine, but the changes were not significant. Thus, neurological response to tilt is not uniform in patients with orthostatic hypotension. Patients with histories of cerebrovascular accidents and patients with Parkinsonism may have impaired function of central neural mechanisms controlling blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
为评估直立性低血压的发病机制,我们采用功率谱分析方法,通过测量21例直立性低血压患者(平均年龄62±2岁,其中5例有脑血管意外病史,5例患有帕金森病,5例患有糖尿病,3例患有嗜铬细胞瘤,3例病因不明)和15名正常健康受试者(平均年龄63±2岁)在60度被动头高位倾斜过程中的心率变异性,对自主调节系统进行了研究。我们还评估了倾斜试验中血浆肾上腺素和去甲肾上腺素的反应。在倾斜过程中,对照受试者心率增加而血压无变化。心率变异性的频谱分析显示低频带(LFB,主要为交感神经)和低频带/高频带比值(LFB/HFB,交感-迷走平衡)增加。所有直立性低血压患者均出现血压显著下降伴心率增加。有脑血管意外病史和帕金森病的患者,LFB和LFB/HFB比值未增加。然而,其他直立性低血压患者在倾斜过程中LFB和LFB/HFB比值增加。去甲肾上腺素在对照受试者以及患有糖尿病、嗜铬细胞瘤和病因不明的患者中增加。相比之下,有脑血管意外病史的患者和帕金森病患者去甲肾上腺素未增加。肾上腺素反应与去甲肾上腺素反应平行,但变化不显著。因此,直立性低血压患者对倾斜的神经反应并不一致。有脑血管意外病史的患者和帕金森病患者可能存在控制血压的中枢神经机制功能受损。(摘要截选至250词)