title: Epinephrine, vasodilation and hemoconcentration in syncopal, healthy men and women.
abstract: Healthy young people may become syncopal during standing, head up tilt (HUT) or lower body negative pressure (LBNP). To evaluate why this happens we measured hormonal indices of autonomic activity along with arterial pressure (AP), heart rate (HR), stroke volume (SV), cardiac output (CO), total peripheral resistance (TPR) and measures of plasma volume. Three groups of normal volunteers (n = 56) were studied supine, before and during increasing levels of orthostatic stress: slow onset, low level, lower body negative pressure (LBNP) (Group 1), 70 degrees head up tilt (HUT) (Group 2) or rapid onset, high level, LBNP (Group 3). In all groups, syncopal subjects demonstrated a decline in TPR that paralleled the decline in AP over the last 40 s of orthostatic stress. Ten to twenty seconds after the decline in TPR. HR also started to decline but SV increased, resulting in a net increase of CO during the same period. Plasma volume (PV, calculated from change in hematocrit) declined in both syncopal and nonsyncopal subjects to a level commensurate with the stress, i.e. Group 3 > Group 2 > Group 1. The rate of decline of PV, calculated from the change in PV divided by the time of stress, was greater (p < 0.01) in syncopal than in nonsyncopal subjects. When changes in vasoactive hormones were normalized by time of stress, increases in norepinephrine (p < 0.012, Groups 2 and 3) and epinephrine (p < 0.025, Group 2) were greater and increases in plasma renin activity were smaller (p < 0.05, Group 2) in syncopal than in nonsyncopal subjects. We conclude that the presyncopal decline in blood pressure in otherwise healthy young people resulted from declining peripheral resistance associated with plateauing norepinephrine and plasma renin activity, rising epinephrine and rising blood viscosity. The increased hemoconcentration probably reflects increased rate of venous pooling rather than rate of plasma filtration and, together with cardiovascular effects of imbalances in norepinephrine, epinephrine and plasma renin activity may provide afferent information leading to syncope.
authors.affiliation: Center for Biomedical Engineering and Division of Cardiology, University of Kentucky, Lexington 40506-0070, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Evans
authors.forename: F M
authors.initials: FM
authors.lastname: Leonelli
authors.forename: M G
authors.initials: MG
authors.lastname: Ziegler
authors.forename: C M
authors.initials: CM
authors.lastname: McIntosh
authors.forename: A R
authors.initials: AR
authors.lastname: Patwardhan
authors.forename: A C
authors.initials: AC
authors.lastname: Ertl
authors.forename: C S
authors.initials: CS
authors.lastname: Kim
authors.forename: C F
authors.initials: CF
authors.lastname: Knapp
mesh_terms: D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D004837:Epinephrine / Q000097:blood*; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006400:Hematocrit; D006801:Humans; D007024:Hypotension, Orthostatic / Q000503:physiopathology; D015994:Incidence; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010191:Pancreatic Polypeptide / Q000097:blood; D010953:Plasma Volume / Q000502:physiology; D012083:Renin / Q000097:blood; D013312:Stress, Physiological / Q000503:physiopathology; D013575:Syncope / Q000453:epidemiology / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D010191:Pancreatic Polypeptide; D012083:Renin; D009638:Norepinephrine; D004837:Epinephrine