Epinephrine, vasodilation and hemoconcentration in syncopal, healthy men and women

Healthy young people may become syncopal during standing, head up tilt (HUT ) or lower body negative pressure (LBNP). To evaluate why this happens we m easured hormonal indices of autonomic activity along with arterial pressure (AP), heart rate (HR), stroke volume (SV), cardiac output (CO), total peri pheral resistance (TPR) and measures of plasma volume. Three groups of norm al volunteers (n = 56) were studied supine, before and during increasing le vels of orthostatic stress: slow onset, low level, lower body negative pres sure (LBNP) (Group 1), 70 degrees head up tilt (HUT) (Group 2) or rapid ons et, high level, LBNP (Group 3). In all groups, syncopal subjects demonstrat ed a decline in TPR that paralleled the decline in A-P over the last 40 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 dur ing the same period. Plasma volume (PV, calculated from change in hematocri t) declined in both syncopal and nonsyncopal subjects to a level commensura te 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 subj ects. 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 wer e smaller (p < 0.05, Group 2) in syncopal than in nonsyncopal subjects. We conclude that the presyncopal decline in blood pressure in otherwise hea lthy young people resulted from declining peripheral resistance associated with plateauing norepinephrine and plasma renin activity, rising epinephrin e and rising blood viscosity. The increased hemoconcentration probably refl ects 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 lea ding to syncope. (C) 2001 Elsevier Science B.V. All rights reserved.