NEUROHUMORAL ANTECEDENTS OF VASODEPRESSOR REACTIONS

Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people du ring exposure to stimuli decreasing cardiac filling. Antecedent physio logical or neuroendocrine conditions for this dramatic syndrome are po orly understood. This study compared neurocirculatory responses to non -hypotensive lower body negative pressure (LBNP) in subjects who subse quently developed vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -1 5 and -40 mmHg was applied to inhibit cardiopulmonary and arterial bar oreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -40 mmHg 11 subjects had vasodepressor reac tions, with sudden hypotension, nausea, and dizziness. In these subjec ts, arterial plasma adrenaline responses to LBNP both at -15 and at -4 0 mmHg exceeded those in subjects who did not experience these reactio ns. In 16 of the 26 subjects, forearm noradrenaline spillover was meas ured; in the eight subjects with a vasodepressor reaction, mean forear m noradrenaline spillover failed to increase during LBNP at -15 mmHg ( Delta = -0.06 +/- (SEM) 0.04 pmol min(-1) 100 mL(-1)), whereas in the eight without a vasodepressor reaction, mean noradrenaline spillover i ncreased significantly (Delta = 0.31 +/- 0.13 pmol min(-1) 100 mL(-1)) . Plasma levels of beta-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LB NP at -40 mmHg. The findings suggest that a neuroendocrine pattern inc luding adrenomedullary stimulation, skeletal sympathoinhibition, and r elease of endogenous opioids can precede vasodepressor syncope.