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Changes in stroke volume directly alter carotid artery distortion during upright posture in humans
Author(s) -
Hastings Jeff,
Shibata Shigeki,
Shook Robin,
Okazaki Kazunobu,
Conner Colin,
Palmer M. Dean,
Fu Qi,
Levine Benjamin D.
Publication year - 2006
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.20.5.lb37-c
Subject(s) - supine position , stroke volume , medicine , cardiology , diastole , blood pressure , systole , heart rate , stroke (engine) , end systolic volume , common carotid artery , carotid arteries , cardiac cycle , pulse pressure , physics , thermodynamics
We tested the hypothesis that changes in stroke volume can directly alter carotid artery distortion during orthostasis in humans. Carotid distortion was quantified using high resolution ultrasonography to measure both systolic and diastolic diameters and wall thickness in the supine position as well as during a graded (30° and 60°) head‐up tilt (HUT) in 5 healthy young subjects. Blood pressure, cardiac output (C 2 H 2 rebreathing), and heart rate were measured, allowing for determination of stroke volume (SV). An index of carotid distortion was calculated, based on the equation for hoop stress of a thin walled vessel, by Δ P·Δ r/t avg (Δ P=hydrostatically corrected carotid pulse pressure, Δ r=difference is measured radius from systole to diastole, and t=average wall thickness measured during systole and diastole). Carotid distortion decreased progressively during graded HUT (mean±SD, 11.1±5.8; 8.1±2.2, 6.2±2.9 mmHg, P =0.039), as did SV (100±23 supine vs. 77±30 and 65±22 ml, P =0.006). The index of carotid distortion was positively correlated to changes in SV during changes in posture ( r =0.671, P =0.006). These preliminary results suggest that changes in stroke volume directly cause changes in carotid artery distortion during orthostasis. These results will lead to further study of SV related sympathetic activation and baroreflex sensitivity in humans. Supported by NIH K23 (HL0752 83) and the GCRC grant (RR00633).

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