Jern S, Bergbrant A, Hedner T, Hansson L
Department of Clinical Physiology, Ostra Hospital, Gothenburg, Sweden.
J Hypertens. 1995 Jan;13(1):69-79.
It has been suggested that the blood pressure elevation in borderline hypertension is caused by hyperreactivity to stress. We addressed the questions: are subjects with borderline hypertension hyperreactive to mental stress, and, if so, is this reflected in greater blood pressure responses during daily-life activities, and does non-specific pressor amplification by structural vascular changes contribute to reactivity changes?
Standardized mental stress was performed during invasive monitoring in 54 borderline hypertensive subjects [systolic blood pressure (SBP) 140-160 or diastolic blood pressure (DBP) 84-95 mmHg, or both] and 20 normotensive control subjects (110-130/60-80 mmHg). Sixteen borderline hypertensive subjects had a cardiac index greater than the mean + 1SD of the normotensive control group (hyperkinetic subgroup) and 38 borderline hypertensive subjects had a cardiac index below that level (normokinetic subgroup). Minimal vascular resistance in the forearm and calf was assessed by plethysmography. Ambulatory 24-h blood pressure was recorded.
Subjects with hyperkinetic borderline hypertension had similar intra-arterial blood pressure levels to normokinetic borderline hypertensive subjects. Total peripheral resistance was lower in hyperkinetic borderline hypertensive than in normokinetic borderline hypertensive or normotensive control subjects. Hyperkinetic borderline hypertensive subjects had a significantly lower forearm minimal vascular resistance than normokinetic borderline hypertensive subjects. SBP and mean arterial blood pressure responses to stress were augmented in both borderline hypertensive subgroups. Hyperkinetic borderline hypertensive subjects also showed diastolic hyperreactivity in response to mental stress, in comparison both with normokinetic borderline hypertensive and with normotensive control subjects. During ambulatory blood pressure recording, hyperkinetic borderline hypertensive subjects had greater DBP and mean blood pressure increases from night to day than normotensive control and normokinetic borderline hypertensive subjects.
Borderline hypertension is characterized by pressor hyperreactivity to mental stress. In hyperkinetic borderline hypertensive subjects, stress hyperresponsiveness is also reflected by greater night-to-day blood pressure gradients during 24-h monitoring. Pressor hyperreactivity in hyperkinetic borderline hypertension is not explained by structural changes in the calf or forearm vasculature.
有人提出临界高血压患者的血压升高是由对应激的高反应性所致。我们探讨了以下问题:临界高血压患者对精神应激是否具有高反应性?如果是,这是否在日常生活活动中表现为更大的血压反应?血管结构改变导致的非特异性升压放大是否会导致反应性变化?
对54名临界高血压患者[收缩压(SBP)140 - 160或舒张压(DBP)84 - 95 mmHg,或两者兼有]和20名血压正常的对照者(110 - 130/60 - 80 mmHg)在有创监测期间进行标准化精神应激测试。16名临界高血压患者的心指数高于血压正常对照组的均值 + 1标准差(高动力亚组),38名临界高血压患者的心指数低于该水平(正常动力亚组)。通过体积描记法评估前臂和小腿的最小血管阻力。记录24小时动态血压。
高动力型临界高血压患者的动脉内血压水平与正常动力型临界高血压患者相似。高动力型临界高血压患者的总外周阻力低于正常动力型临界高血压患者或血压正常的对照者。高动力型临界高血压患者的前臂最小血管阻力显著低于正常动力型临界高血压患者。两个临界高血压亚组对应激的收缩压和平均动脉血压反应均增强。与正常动力型临界高血压患者和血压正常的对照者相比,高动力型临界高血压患者对精神应激也表现出舒张期高反应性。在动态血压记录期间,高动力型临界高血压患者夜间到白天的舒张压和平均血压升高幅度大于血压正常的对照者和正常动力型临界高血压患者。
临界高血压的特征是对应激的升压高反应性。在高动力型临界高血压患者中,应激高反应性在24小时监测期间也表现为更大的夜间到白天血压梯度。高动力型临界高血压患者的升压高反应性不能用小腿或前臂血管结构的改变来解释。