Neurohumoral antecedents of vasodepressor reactions

Abstract

Abstract. Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine condi tions for this dramatic syndrome are poorly under stood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently devel oped vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40 mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -4 0 mmHg 11 subjects had vasodepressor reac tions, with sudden hypotension, nausea, and dizzi ness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15mmHg (A^-0*06± (S E M ) 0*04pmol m in'1100 mL" 1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (A = 0*31 ±0* 13 pmol m in '1 lOOmL" 1). Plasma levels of /?-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40 mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinbibition, and release of endogenous opioids can precede vasode pressor syncope.

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

“…The concomitant presence of hypotension and inadequate HR response indicate that the normal baroreflex function has been superseded. Some authors have proposed that "sudden" resetting baroreflexes results in sympathoneural withdrawal despite significant hypotension (13). Our results now clearly document that an underlying baroreceptor reflex dysfunction leads to a defective sympathetic response to orthostatic stress in patients with recurrent syncope.…”

“…This was then followed by progressive MSNA inhibition until complete disappearance and syncope. Attempts to evaluate sympathetic function with plasma NorEpi in neurally mediated syncope have produced variable and seemingly contradictory results; NorEpi concentrations have been reported to be either relatively low (13,26,27), normal (28), or moderately elevated (4,29,30). Confounding factors such as time of sampling, potential changes in NorEpi clearance, and alterations in spillover to the general circulation are likely to account for these contradictory results (17,31).…”

“…Confounding factors such as time of sampling, potential changes in NorEpi clearance, and alterations in spillover to the general circulation are likely to account for these contradictory results (17,31). More recently, Jacobs and collaborators have documented a blunted noradrenergic response combined with exaggerated adrenomedullary activation in subjects who subsequently developed vasodepressor reactions during exposure to pronounced lower body negative pressure (13).…”

“…Stimulation of these afferents may result in reflex vasodilation with or without bradycardia (10)(11)(12). Alternatively, others have proposed that a sudden central resetting of baroreflexes produces loss of sympathetic vascular control with subsequent syncope (13).…”

Neurocirculatory Abnormalities in Chronic Orthostatic Intolerance

“…34 This attenuation can help explain relatively small increments in forearm vascular resistance during orthostasis or lower-body negative pressure in NCS patients, as noted previously 34 -36 and confirmed in the present study.…”