ROLE OF ENDOGENOUS OPIOIDS AND CATECHOLAMINES IN VASOVAGAL SYNCOPE

Head-up tilt testing demonstrates vasovagal mechanisms as a cause for syncope, but the pathophysiology underlying this condition remains unc lear. The aim of this study was (i) to measure plasma beta-endorphins, adrenocorticotrophic hormone, cortisol, catecholamines: and brain nat riuretic peptide during head-up tilt, and (ii) to assess the effect of naloxone infusion during head-up tilt in subjects with reproducible v asovagal syncope. During the assessment of unexplained syncope, 71 sub jects underwent a total of 93 tilt tests (60-70 degrees head upwards f or 40-45 min or until syncope occurred) during which frequent blood sa mpling was performed. Subjects with a positive tilt test (n=56) (mean duration to syncope 23.6 min) showed a larger rise in beta-endorphin l evels prior to syncope (baseline 4.7 +/- 2.2 vs syncope onset 6.9 +/- 3.2 pmol.l(-1), P=0.0001) than those with a negative test (n=37) (base line 3.9 +/- 3.9 vs end of rest 4.9 +/- 2.3 pmol.l(-1), P=0.03). Durin g tilting, adrenocorticotrophic hormone, cortisol, and noradrenaline i ncreased; adrenaline and brain natriuretic peptide remained unchanged; and these responses were similar in positive and negative test groups . Naloxone (2.6 mg.kg(-1) i.v. bolus followed by 20 mu g.kg(-1).min(-1 ) infusion), administered in a double-blind fashion during head-up til t in nine subjects, failed to modify either the time to syncope or the vasodepressor response. Thus, endogenous opioids appear not to be an important trigger for vasovagal syncope, and other pathophysiological mechanisms should be considered.