title: Triggering mechanism for neurally mediated syncope induced by head-up tilt test: role of catecholamines and response to propranolol.
abstract: OBJECTIVE
  We studied the triggering mechanism for neurally mediated syncope.
  
  
  BACKGROUND
  Although increased transient sympathetic tone is thought to be necessary for the development of neurally mediated syncope, little is known about the triggering mechanism for neurally mediated syncope.
  
  
  METHODS
  Plasma epinephrine (EP) and norepinephrine (NE) levels were assessed in 20 syncope patients during tilt test (80 degrees, 15 min) with and without isoproterenol (ISP, 0.01, 0.02 microg/kg/min). If syncope occurred, propranolol (0.1 mg/kg) was injected.
  
  
  RESULTS
  Eight patients experienced syncope during tilting alone, and 9 patients required ISP for syncope. In the negative response without ISP, NE showed a small statistical 1.7-fold increase at end of tilting and EP did not change during tilting. When syncope occurred during tilting alone, a significant 11.7-fold increase in EP at syncope was registered concomitant with a small 2.5-fold increase in NE. When patients experienced syncope during tilting with ISP, a significant 5.0-fold increase in EP at syncope was registered concomitant with a small 1.7-fold increase in NE. In patients without ISP, propranolol did not interrupt syncope. In patients with ISP, six of eight receiving propranolol responded to tilting negatively.
  
  
  CONCLUSIONS
  An increase of NE levels may result in inhibition of syncope and an EP surge may be a triggering mechanism for neurally mediated syncope. Comparatively low levels of EP may be enough to induce syncope during tilting with ISP compared with tilting alone. Propranolol is not effective in patients without ISP, but it frequently inhibits syncope in patients with ISP. Propranolol (0.1 mg/kg) may be insufficient to block the actions of high levels of circulating EP.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Kikushima
authors.forename: Y
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: H
authors.initials: H
authors.lastname: Nakagawa
authors.forename: T
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000293:Adolescent; D000313:Adrenal Medulla / Q000378:metabolism; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000328:Adult; D002395:Catecholamines / Q000097:blood*; D004562:Electrocardiography; D004837:Epinephrine / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D011433:Propranolol / Q000627:therapeutic use*; D015203:Reproducibility of Results; D013564:Sympathetic Nervous System / Q000378:metabolism; D013575:Syncope / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D018667:Tilt-Table Test / Q000009:adverse effects*