Cardiovascular effects of noise.

The purpose of this study was to evaluate the acute hemodynamic and hormonal effects induced by short-term exposure to loud noise in man. Loud noise (95 dBA or 100 dBA) caused an increase in blood-pressure in healthy normotensive subjects as well as in patients with essential hypertension. The blood pressure elevation was caused by vasoconstriction in patients with essential hypertension and in normotensive subjects with a positive family history of hypertension, while the blood pressure response in normotensive subjects without a family history of hypertension was due mainly to an increase in cardiac output. This might indicate that there are genetically determined differences in the cardiovascular response to noise. Stimulation with noise did not increase plasma levels of catecholamines, prolactin, cortisol or growth in normotensive subjects. In patients with essential hypertension plasma noradrenalin increased, while plasma adrenalin and plasma renin activity did not change. The increase in diastolic blood pressure caused by loud noise was not affected by beta 1-selective or non-selective beta-adrenoceptor blockade, nor was it changed by alpha 1-or combined alpha 1-and non-selective beta-adrenoceptor blockade. The elevation in blood pressure induced by noise is usually mediated by vasoconstriction, i.e. an alpha 1-effect. When alpha 1-adrenoceptors are blocked, the blood pressure response to noise is mediated by an increase in cardiac output, i.e. a beta-adrenoceptor mediated effect. It thus seems as if an increased pressure is essential during exposure to loud noise. If one part of the sympathetic nervous system is blocked, other parts can be activated in order to preserve the blood pressure on an elevated level. This indicates a temporary resetting of the baroreceptors during exposure to noise, which probably is mediated from the hypothalamus.

RCT Entities:   Population Interventions Outcomes