[Show abstract][Hide abstract] ABSTRACT: The mechanism of alcohol-induced syncope is unknown.
Head-up tilt tests (HUT: upright at 80 degrees for 30 min) were performed before and after alcohol consumption in 25 patients with unexplained syncope after drinking alcohol. Plasma levels of epinephrine (P-E) and norepinephrine (P-NE) were measured in a supine position and during HUT (at 15 min). Before drinking alcohol, HUT did not provoke neurocardiogenic syncope (NCS) in any of the 25 patients. After drinking alcohol, HUT provoked NCS in 11 patients (alcohol-positive or AP group) but not in 14 patients (alcohol-negative or AN group). Prior to alcohol consumption, P-E and P-NE increased during HUT in both groups, and did not differ significantly between the 2 groups. After alcohol consumption, P-E and P-NE increased during HUT in both group. During HUT, P-NE did not differ between the 2 groups, but P-E was significantly higher in the AP group than in the AN group during HUT (258.0+/-179.2 vs 70.9+/-35.1 pg/ml, p<0.05).
These results suggest that an imbalance in the increases of adrenomedullar sympathetic nerve activity (as expressed by the P-E level) and peripheral sympathetic nerve activity (as expressed by the P-NE level) both induced by alcohol, may play a crucial role in alcohol-induced NCS.
No preview · Article · Jun 2008 · Circulation Journal
[Show abstract][Hide abstract] ABSTRACT: Basic autonomic nervous function was evaluated in patients with neurocardiogenic syncope (NCS). Atropine, isoproterenol, propranolol, phenylephrine, and phentolamine were administered successively, and parasympathetic nerve activity and beta- (and alpha-) activity, sensitivity, and secretion of the sympathetic nerve were determined in patients with NCS and control subjects. In patients with NCS, beta- and alpha- sensitivity were higher and beta-activity and beta- and alpha-secretion lower than in control subjects. In patients with NCS, the increased basic beta-sensitivity may contribute to induce strong cardiac contractions and augment ventricular mechanoreceptor response, and a compensatory state against diminished neuronal sympathetic activity is suggested by the increased alpha-sensitivity.
No preview · Article · May 2007 · Clinical and Experimental Hypertension