NEURAL CONTROL MECHANISMS AND VASOVAGAL SYNCOPE

Patients with recurrent unexplained syncope may have cardioinhibitory and vasodepressor responses provokable with head-up tilt with or witho ut exogenous beta-adrenergic stimulation. Although these responses are believed to be neurally mediated, the neural mechanisms involved are poorly understood. Numerous studies have documented peripheral vasodil ation, hypotension, and bradycardia at the time of syncope and several case reports have shown sudden withdrawal of vasoconstrictor sympathe tic neural outflow to skeletal muscle in human subjects. In cats and r ats, a similar response can be provoked with hemorrhage and is prevent ed by interruption of cardiac vagal C-fiber afferents. In dogs, howeve r, section of these fibers does not prevent the development of a vasod epressor response. The provocation of vasodepressor syncope during nit roprusside infusion in a heart transplant recipient with presumed vent ricular denervation also suggests that cardiac afferent nerves may not be required for the development of vasodepressor responses in humans. Other potential mechanisms include release of endogenous opioids or n itric oxide that may inhibit sympathetic nerve firing, and primary cen tral nervous system activation (as in partial seizures) that triggers cardioinhibitory and vasodepressor responses. This article reviews our current understanding of the mechanisms involved in the development o f neurally mediated syncope.