Circulatory Effects of Noise

Abstract

Thirteen patients with mild essential hypertension, mean age 44 years (range 21–59), were studied during “stress” before and after postsynaptic α‐adrenoceptor blockade and combined postsynaptic α‐ and non‐selective β‐adrenoceptor blockade. Loud broad band noise (100 dBA for 10 min) was used as the stress stimulus. Exposure to noise caused a significant increase in systolic (7%, p<0.05), diastolic (9%, p<0.01) and mean arterial pressure (6%, p<0.01). The blood pressure elevation was caused by an increase in total peripheral resistance (12%, p<0.05). There was no significant change in heart rate, stroke volume or cardiac output. The blood pressure response during noise stimulation was not affected by postsynaptic α‐adrenoceptor blockade (prazosin, 2 mg orally). The hemodynamic reaction pattern, however, was totally reversed. Thus, the cardiac output increased significantly (9%, p<0.05), while the total peripheral resistance tended to decrease. Combined postsynaptic α‐ and non‐selective β‐adrenoceptor blockade (la‐be talol, 200 mg orally) inhibited the increase in systolic blood pressure caused by noise, while the diastolic and mean arterial pressures still increased significantly (5%, p<0.01). Labetalol effectively blocked the stress‐induced increase in total peripheral resistance and there was no significant increase in cardiac output after combined α‐ and β‐adrenoceptor blockade. Exposure to noise caused a significant increase in circulating noradrenaline (20%, p<0.05). Plasma adrenaline and plasma renin activity were not affected by noise stimulation. These results suggest that blood pressure elevation is essential during “stress” but that the hemodynamic pattern causing blood pressure elevation may vary and may be affected by pharmacological blockade of various parts of the sympathetic nervous system.

Acute effects of noise exposure on 24-h ambulatory blood pressure in hypertensive adults

“…The elevations of ambulatory SBP and DBP caused by a 1-dBA increase in the 24-h average noise exposure among the hypertensive workers during the working and nonworking days supported the results in an experimental study that exposure to 100 dBA for 10 min caused the significant elevations of resting SBP and DBP among 13 patients with mild essential hypertension [26]. However, the differences in the DBP between the hypertensive and normotensive groups during sleep (with a maximum value of 0.06 mmHg in DBP) were obviously lower than those in the SBP (with a maximum value of 0.22 mmHg in SBP).…”

How and why environmental noise impacts animals: an integrative, mechanistic review

“…In the latter instance, it was suggested that the main effect of noise was to disrupt normal hormone release patterns, such that the daily peak occurred later. Increases in noradrenaline levels have been reported for humans (Andrén et al. 1983), rats (Lenzi et al.…”

“…As with research on the HPA axis, the bulk of cardiovascular studies have focused on humans, rats and mice. Among humans, exposure to loud noise (both temporary and long‐term), is associated with increases in systolic, diastolic and main arterial pressures, leading to an increase in total peripheral resistance to blood flow (Andrén et al. 1983).…”

Vulnerability of bus and truck drivers affected from vehicle engine noise

“…Noise, defined as undesirable sound, is unknown to be a stress stimulus (Mondal, 2013) that can produce acute blood pressure (BP) elevation in animals (Baudrie et al, 2001) and humans in laboratory or occupational settings (Andren et al, 1983). Noise is most widely spread pollutant in work environment and living environments (Mondal and Ghatak, 2014;Tomei et al, 2000).…”