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嗜铬细胞瘤患者心血管系统交感神经和迷走神经调节的改变:它们与直立性低血压的关系。

Altered sympathetic and vagal modulations of the cardiovascular system in patients with pheochromocytoma: their relations to orthostatic hypotension.

作者信息

Munakata M, Aihara A, Imai Y, Noshiro T, Ito S, Yoshinaga K

机构信息

Division of Hypertension and Cardiology, Tohoku Rosai Hospital, Sendai, Japan.

出版信息

Am J Hypertens. 1999 Jun;12(6):572-80. doi: 10.1016/s0895-7061(99)00026-6.

Abstract

To examine sympathetic and vagal cardiovascular regulatory mechanisms in the pathogenesis of orthostatic hypotension in pheochromocytoma, we continuously monitored blood pressure (Finapres) and RR interval (electrocardiogram) in supine and standing positions in 12 patients with pheochromocytoma, 43 patients with essential hypertension, and 30 normotensive subjects. Mayer wave power spectrum of systolic blood pressure variability (approximately 0.1 Hz) and respiratory power spectrum of the RR interval variability (approximately 0.25 Hz) were taken as measures of sympathetic vascular and cardiac vagal modulations, respectively. Systolic blood pressure decreased more upon standing in pheochromocytoma patients (-21 +/- 7 mm Hg) than in normotensive subjects (-5 +/- 2 mm Hg) or essential hypertensive patients (-3 +/- 2 mm Hg) (P < .005 for both), whereas heart rate tended to increase most in the pheochromocytoma group. Postural reduction in systolic blood pressure was highly correlated with postural increase in heart rate (reciprocal change in RR interval) in the pheochromocytoma group (r = 0.716, P < .01) suggesting that baroreflex is well functioning in those patients. The Mayer wave power spectrum in recumbency was extremely depressed in pheochromocytoma patients (1.1 +/- 0.2 mm Hg2) compared with normotensives (4.5 +/- 0.8 mm Hg2) or essential hypertensives (5.6 +/- 0.6 mm Hg2) (P < .001 for both). This parameter increased significantly with standing in all groups but remained lower in patients with pheochromocytoma (5.1 +/- 1.0 mm Hg2) than in normotensives (7.1 +/- 0.9 mm Hg2, P = NS), whereas essential hypertensive patients demonstrated far greater value (19.2 +/- 3.8, P < .01 for both). The respiratory power spectrum of the RR interval in recumbency of pheochromocytoma patients (189 +/- 54 msec2) was less than in normotensive subjects (714 +/- 100 msec2, P < .001) but did not differ from that in patients with essential hypertension (214 +/- 41 msec2). The respiratory power spectrum of the RR interval upon standing was markedly suppressed in pheochromocytoma patients (36.9 +/- 16.7 msec2) compared with normotensive subjects (129.5 +/- 23.6 msec2) or essential hypertensive patients (126.6 +/- 28.6 msec2) (P < .001 for both). Postural decrement in the respiratory power spectrum of the RR interval correlated positively with postural increase in heart rate (r = 0.577, P < .05) in patients with pheochromocytoma. After successful surgery (n = 9), the Mayer wave power spectrum of the systolic blood pressure and the blood pressure response to orthostasis were normalized. These data suggest that altered sympathetic vascular regulation is central to the pathogenesis of orthostatic hypotension in pheochromocytoma, whereas cardiac vagal regulation acts to compensate.

摘要

为研究嗜铬细胞瘤体位性低血压发病机制中的交感神经和迷走神经心血管调节机制,我们持续监测了12例嗜铬细胞瘤患者、43例原发性高血压患者和30例血压正常者仰卧位和站立位时的血压(Finapres)和RR间期(心电图)。收缩压变异性的迈尔波功率谱(约0.1Hz)和RR间期变异性的呼吸功率谱(约0.25Hz)分别作为交感神经血管调节和心脏迷走神经调节的指标。嗜铬细胞瘤患者站立时收缩压下降幅度(-21±7mmHg)大于血压正常者(-5±2mmHg)或原发性高血压患者(-3±2mmHg)(两者P均<0.005),而嗜铬细胞瘤组心率升高幅度最大。嗜铬细胞瘤组站立时收缩压的降低与心率的升高(RR间期的反向变化)高度相关(r=0.716,P<0.01),提示这些患者压力反射功能良好。与血压正常者(4.5±0.8mmHg2)或原发性高血压患者(5.6±0.6mmHg2)相比,嗜铬细胞瘤患者卧位时的迈尔波功率谱极低(1.1±0.2mmHg2)(两者P均<0.001)。该参数在所有组中站立时均显著升高,但嗜铬细胞瘤患者(5.1±1.0mmHg2)仍低于血压正常者(7.1±0.9mmHg2,P=无显著性差异),而原发性高血压患者的值则高得多(19.2±3.8,两者P<0.01)。嗜铬细胞瘤患者卧位时RR间期的呼吸功率谱(189±54msec2)低于血压正常者(714±100msec2,P<0.001),但与原发性高血压患者(214±41msec2)无差异。与血压正常者(129.5±23.6msec2)或原发性高血压患者(126.6±28.6msec2)相比,嗜铬细胞瘤患者站立时RR间期的呼吸功率谱显著降低(36.9±16.7msec2)(两者P<0.001)。嗜铬细胞瘤患者RR间期呼吸功率谱的体位性降低与心率的体位性升高呈正相关(r=0.577,P<0.05)。9例患者成功手术后,收缩压的迈尔波功率谱和体位性低血压反应恢复正常。这些数据表明,交感神经血管调节改变是嗜铬细胞瘤体位性低血压发病机制的核心,而心脏迷走神经调节起代偿作用。

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