S Holand1, A Girard, D Laude, C Meyer-Bisch, J L Elghozi. 1. Centre d'Investigation Clinique, Association Claude Bernard, Assistance Publique--Hôpitaux de Paris, Hôpital Necker--Enfants Malades, Paris, France.
Abstract
OBJECTIVE: To describe the effects of an auditory startle stimulus on blood pressure (BP) and heart rate (HR) in humans. DESIGN AND METHODS: Twenty-five volunteers, including nine untreated hypertensive subjects, were studied in the supine position. Polygraphic recordings were obtained for finger BP, R-R interval using ECG, respiratory movements using a thoracoabdominal belt and for electrooculomyogram using adhesive electrodes. Haemodynamic estimations were derived by modelling flow from the noninvasive BP signal. A background noise of 55 dB was administered through headphones and two acoustic startle stimuli (110 dB, 1-20 kHz, 0.15 s) were generated at 5-min intervals during the tele-expiratory phase. The sham stimulation (0 dB, event marker) was compared with the effects of the noise stimulus (one-way ANOVA with repeated measures followed by a protected t test for multiple comparisons). RESULTS: A biphasic cardiovascular profile was observed in response to noise stimulation. Blood pressure and HR increases were combined in the early response (0-10 s) observed after the immediate motor contraction (blink). The average systolic BP rise was 18.7+/-2.7 mmHg (peak at 5.1 s) and the average HR increase was 10.8+/-1.1 bpm (peak at 3.4 s) for the first stimulus. These effects were highly significant compared with the sham response (P < 0.01). The second stimulus elicited BP and HR rises of a lesser amplitude (P < 0.01). The delayed response (10-30 s) corresponded with a moderate BP decrease. The haemodynamic indexes suggest that the early rise in blood pressure reflects a rise in total peripheral resistance. CONCLUSION: This is the first description of the BP response to an acute loud noise in humans. The early (within 10 s) BP and HR rises may depend upon the autonomic component of the startle reflex. One application of this test could be the discrimination of the different classes of antihypertensive drugs according to their sites of action.
OBJECTIVE: To describe the effects of an auditory startle stimulus on blood pressure (BP) and heart rate (HR) in humans. DESIGN AND METHODS: Twenty-five volunteers, including nine untreated hypertensive subjects, were studied in the supine position. Polygraphic recordings were obtained for finger BP, R-R interval using ECG, respiratory movements using a thoracoabdominal belt and for electrooculomyogram using adhesive electrodes. Haemodynamic estimations were derived by modelling flow from the noninvasive BP signal. A background noise of 55 dB was administered through headphones and two acoustic startle stimuli (110 dB, 1-20 kHz, 0.15 s) were generated at 5-min intervals during the tele-expiratory phase. The sham stimulation (0 dB, event marker) was compared with the effects of the noise stimulus (one-way ANOVA with repeated measures followed by a protected t test for multiple comparisons). RESULTS: A biphasic cardiovascular profile was observed in response to noise stimulation. Blood pressure and HR increases were combined in the early response (0-10 s) observed after the immediate motor contraction (blink). The average systolic BP rise was 18.7+/-2.7 mmHg (peak at 5.1 s) and the average HR increase was 10.8+/-1.1 bpm (peak at 3.4 s) for the first stimulus. These effects were highly significant compared with the sham response (P < 0.01). The second stimulus elicited BP and HR rises of a lesser amplitude (P < 0.01). The delayed response (10-30 s) corresponded with a moderate BP decrease. The haemodynamic indexes suggest that the early rise in blood pressure reflects a rise in total peripheral resistance. CONCLUSION: This is the first description of the BP response to an acute loud noise in humans. The early (within 10 s) BP and HR rises may depend upon the autonomic component of the startle reflex. One application of this test could be the discrimination of the different classes of antihypertensive drugs according to their sites of action.
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