Lindvall K, Kahan T, de Faire U, Ostergren J, Hjemdahl P
Department of Medicine, Danderyd Hospital, Stockholm, Sweden.
Clin Cardiol. 1991 Feb;14(2):125-32. doi: 10.1002/clc.4960140208.
Left ventricular function was studied by M-mode echocardiography at rest and during a mental arithmetic stress test and a cold-pressor test in 14 patients with mild hypertension and in 14 matched normotensive subjects. The elevation of blood pressure at rest in the hypertensive group (154 +/- 4/87 +/- 3 vs. 120 +/- 3/66 +/- 3 mmHg in the control group) was due mainly to a higher cardiac output (6.0 +/- 0.3 vs. 5.0 +/- 0.3 L/min), which was related to elevations of stroke volume and heart rate (73 +/- 2 vs. 66 +/- 2 beats/min). Venous plasma catecholamines were similar in the two groups. Mental stress induced cardiac output-dependent increases in blood pressure in both groups; systemic vascular resistance tended to decrease. The relative increases in diastolic and mean arterial blood pressure were smaller in the hypertensive group (15 vs. 26% and 15 vs. 21%, respectively), which exhibited signs of a reduced cardiac compliance, possibly related to a left ventricular hypertrophy. Mental stress elevated venous plasma adrenaline similarly in the two groups; effects on noradrenaline were small. The cold-pressor test increased blood pressure similarly in the two groups, largely due to increased systemic vascular resistance; plasma noradrenaline responses were also similar. Mental stress appears to elicit a differentiated sympathetic nerve activation pattern resembling the hypothalamic defense reaction. Mild hypertension seems to be associated with increased arousal and cardiac activation at rest. However, an attenuated blood pressure reactivity to mental stress may reflect reduced stroke volume responsiveness, which is related to structural changes, as heart rate reactivity tended to be enhanced in mild hypertension.
对14例轻度高血压患者和14例年龄、性别匹配的血压正常者,采用M型超声心动图在静息状态、心算应激试验及冷加压试验时研究左心室功能。高血压组静息血压升高(154±4/87±3 mmHg,对照组为120±3/66±3 mmHg)主要是由于心输出量增加(6.0±0.3 vs. 5.0±0.3 L/min),这与每搏输出量和心率升高有关(73±2 vs. 66±2次/分钟)。两组静脉血浆儿茶酚胺水平相似。精神应激使两组血压随的心输出量增加而升高;全身血管阻力有降低趋势。高血压组舒张压和平均动脉压的相对升高幅度较小(分别为15%对26%和15%对21%),提示心脏顺应性降低,可能与左心室肥厚有关。两组精神应激时静脉血浆肾上腺素升高程度相似;对去甲肾上腺素的影响较小。冷加压试验使两组血压升高程度相似,主要是由于全身血管阻力增加;血浆去甲肾上腺素反应也相似。精神应激似乎引发了一种类似于下丘脑防御反应的交感神经激活模式的分化。轻度高血压似乎与静息时觉醒增加和心脏激活有关。然而,对精神应激的血压反应减弱可能反映了每搏输出量反应性降低,这与结构改变有关,因为轻度高血压时心率反应性往往增强。