Rüddel H, Langewitz W, Schächinger H, Schmieder R, Schulte W
Department of Medicine, University of Bonn, West Germany.
Am Heart J. 1988 Aug;116(2 Pt 2):617-27. doi: 10.1016/0002-8703(88)90560-1.
Stress has been identified as contributing to the development of cardiovascular disease. The pathophysiologic link between stress and disease still remains unclear. Because experimental stress testing in the laboratory permits the examination of the underlying mechanism for stress-induced blood pressure, analyses of cardiovascular reactivity during emotional stress could be of particular clinical importance. The analyses of pooled data during the past 6 years (n = 298, age from 20 to 60 years, normotensive subjects as well as patients with borderline and mild essential hypertension) reveal that stress-induced changes in stroke volume and especially in total peripheral resistance are crucial parameters to analyze the hemodynamic stress response. However, neither those simple nor complex response patterns such as "hot reactor" describe clinically distinct subgroups of persons. When physiologic testing was repeated in hypertensive patients after effective long-term antihypertensive therapy with clonidine, oxprenolol, nitrendipine, or enalapril, no attenuation of the stress-induced increase in blood pressure was found in any of these groups. However, heart rate reactivity and stress-induced changes in total peripheral resistance were altered significantly by oxprenolol and nitrendipine. The beta-adrenoceptor blocker decreased heart rate reactivity and increased reactivity of peripheral resistance; the calcium antagonist decreased stress-induced changes in peripheral resistance and increased the heart rate response. The centrally acting sympatholytic regimen and the angiotensin-converting enzyme inhibitor had no impact on the hemodynamic response pattern during emotional challenge.
压力已被确认为导致心血管疾病的一个因素。压力与疾病之间的病理生理联系仍不清楚。由于实验室中的实验性压力测试能够检查压力诱导血压的潜在机制，因此分析情绪压力期间的心血管反应性可能具有特殊的临床重要性。对过去6年汇总数据的分析（n = 298，年龄在20至60岁之间，包括血压正常者以及临界高血压和轻度原发性高血压患者）显示，压力诱导的每搏输出量变化，尤其是总外周阻力变化，是分析血流动力学应激反应的关键参数。然而，无论是简单的还是复杂的反应模式，如“热反应者”，都没有描述出临床上不同的人群亚组。当使用可乐定、氧烯洛尔、尼群地平或依那普利进行有效的长期抗高血压治疗后，对高血压患者重复进行生理测试时，在这些组中均未发现压力诱导的血压升高有所减弱。然而，氧烯洛尔和尼群地平显著改变了心率反应性和压力诱导的总外周阻力变化。β-肾上腺素能受体阻滞剂降低了心率反应性，增加了外周阻力反应性；钙拮抗剂减少了压力诱导的外周阻力变化，增加了心率反应。中枢作用的交感神经阻滞剂方案和血管紧张素转换酶抑制剂对情绪挑战期间的血流动力学反应模式没有影响。
