VASOVAGAL SYNCOPE AND SKELETAL-MUSCLE VASODILATATION - THE CONTINUINGCONUNDRUM

During vasovagal syncope, profound bradycardia and hypotension occur. Atropine administration can prevent the bradycardia but not the hypote nsion, suggesting that marked peripheral vasodilation is a major cause of the fall in arterial pressure. This concept has been confirmed sin ce vasovagal syncope can be seen in patients who have undergone heart transplantation and also in patients subject to cardiac pacing. In bot h cases, there is no bradycardia but hypotension during the syncopal a ttacks. The major site of the vasodilation is in skeletal muscle and m uscle sympathetic nerve activity is suppressed just prior to and durin g vasovagal attacks, indicating that sympathetic withdrawal contribute s to the dilation. However, the skeletal muscle vasodilation seen duri ng syncope is greater than that caused by sympathetic withdrawal alone , and if is absent in limbs that have undergone surgical sympathectomy , or local anesthetic nerve block. These observations suggest a role f or neurally mediated ''active'' vasodilation during syncope. The affer ent neural pathways that evoke the profound vasodilation during vasova gal attacks remain the subject of debate. The neural pathways responsi ble for the active component of the dilation are also unknown. Recent evidence has demonstrated that cholinergic, beta-adrenergic, and nitro xidergic (nitric oxide) vasodilator mechanisms are not essential to ob serve the dilation, demonstrating that the mechanisms responsible for it remain a continuing conundrum.