Eggertsen R, Andrén L, Hansson L
Eur Heart J. 1984 Jul;5(7):556-60. doi: 10.1093/oxfordjournals.eurheartj.a061705.
The effects of acute exposure to noise on central and regional (calf and forearm) haemodynamics were studied during placebo therapy and during combined nonselective beta-adrenoceptor blockade and precapillary vasodilatation in 9 patients with essential hypertension. On placebo therapy a loud noise (105 dBA for 10 min) caused a significant increase in diastolic and mean arterial pressure due to vasoconstriction. There was also a significant increase of vascular resistance in the calf. After combined precapillary vasodilatation and non-selective beta-adrenoceptor blockade, the increase in blood pressure during stimulation with noise was not prevented. Thus, systolic as well as diastolic and mean arterial pressures increased significantly. This indicates a temporary resetting of the baroreceptors, allowing a higher level of blood pressure during stimulation with noise. Such a resetting would involve the central nervous system pathways of the baroreflex and this would explain why the peripherally active therapeutic principle--precapillary vasodilatation and beta-adrenoceptor blockade--was unable to inhibit the blood pressure response induced by noise.
在9例原发性高血压患者中,研究了安慰剂治疗期间以及联合应用非选择性β-肾上腺素能受体阻滞剂和毛细血管前血管扩张剂时,急性暴露于噪声对中枢和局部(小腿和前臂)血流动力学的影响。在安慰剂治疗期间,高强度噪声(105分贝,持续10分钟)因血管收缩导致舒张压和平均动脉压显著升高。小腿血管阻力也显著增加。在联合应用毛细血管前血管扩张剂和非选择性β-肾上腺素能受体阻滞剂后,噪声刺激期间血压升高未得到预防。因此,收缩压以及舒张压和平均动脉压均显著升高。这表明压力感受器出现了暂时重置,使得在噪声刺激期间血压维持在较高水平。这种重置将涉及压力反射的中枢神经系统通路,这就解释了为什么外周活性治疗原则——毛细血管前血管扩张和β-肾上腺素能受体阻滞——无法抑制噪声诱导的血压反应。