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Effect of Ultrasonic Bone Stimulation of the Mastoid on Renal and Coronary Blood Flow in Humans
Author(s) -
Ray Chester,
Park Susie,
Sauder Charity
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.649.3
Subject(s) - medicine , vasoconstriction , blood pressure , blood flow , supine position , heart rate , cardiology , renal blood flow , stimulation , renal circulation , anesthesia
We have previously demonstrated that external stimulation of the otolith organs by ultrasonic bone stimulation (UBS) of the mastoid increases muscle sympathetic nerve activity. These responses are similar to that observed by head‐down rotation. Additionally, stimulation of the vestibulosympathetic reflex by head‐down rotation elicits leg and renal vasoconstriction. The purpose of this study was to determine if UBS elicits vascular changes to the renal and coronary arteries. We hypothesized that UBS would elicit vasoconstriction in the renal but not the coronary vascular bed. Ten subjects (3 F, 7 M; 25±1 yr; 174.0±3.2 cm; 71.8±4.3 kg) performed UBS in the supine position for 3 min during measurement of arterial blood pressure, heart rate, renal blood flow, and coronary blood flow. Blood flow was measured using Doppler ultrasound. UBS did not change mean arterial blood pressure (Δ‐1±1 mmHg) or heart rate (Δ‐1±1 beats/min) from baseline. Renal vascular conductance was significantly decreased from baseline during UBS (0.63±0.03 and 0.60±0.04 cm/s/mmHg, respectively; P=0.02). However, there were no changes in coronary vascular conductance during UBS (0.18±0.01 and 0.18±0.02, for baseline and UBS, respectively). In conclusion, UBS can elicit vasoconstriction of the renal vascular bed similar to that observed during head‐down rotation. This finding suggests that external stimulation of the otolith organs might assist in postural blood pressure regulation in people with decreased orthostatic tolerance. Supported by: NIH R21HL109952