Role of endogenous opioids and catecholamines in vasovagal syncope

• Published in: European heart journal 1996-11, Vol.17 (11), p.1729-1736
• Main Authors: Wallbridge, D. R., Maclntyre, H. E., Gray, C. E., Oldroyd, K. G., Rae, A. P., Cobbe, S. M.
• Format: Article
• Language: English
• Subjects: Adrenocorticotropic Hormone - blood; Adult; Aged; Biological and medical sciences; Blood Pressure - drug effects; catecholamines; Catecholamines - blood; Endorphins - blood; Endorphins - drug effects; Female; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Heart Rate - drug effects; Humans; Hydrocortisone - blood; Male; Medical sciences; Middle Aged; naloxone; Naloxone - pharmacology; Natriuretic Peptide, Brain; Nerve Tissue Proteins - blood; Nervous system (semeiology, syndromes); Neurology; opioids; Space life sciences; Syncope, Vasovagal - diagnosis; Tilt-Table Test - methods; tilt-testing; Vasovagal syncope; β-endorphin
• ISSN: 0195-668X; 1522-9645
• DOI: 10.1093/oxfordjournals.eurheartj.a014758

Head-up tilt testing demonstrates vasovagal mechanisms as a cause for syncope, but the pathophysiology underlying this condition remains unclear. The aim of this study was (i) to measure plasma β-endorphins, adrenocorticotrophic hormone, cortisol, catecholamines, and brain natriuretic peptide during head-up tilt, and (ii) to assess the effect of naloxone infusion during head-up tilt in subjects with reproducible vasovagal syncope. During the assessment of unexplained syncope, 71 subjects underwent a total of 93 tilt tests (60–70° head upwards for 40–45 min or until syncope occurred) during which frequent blood sampling was performed. Subjects with a positive tilt test (n=56) (mean duration to syncope 23.6 min) showed a larger rise in β-endorphin levels prior to syncope (baseline 4.7 ± 2.2 vs syncope onset 6.9 ± 3.2 pmol . 1−1, P=0.0001) than those with a negative test (n=37) (baseline 39 ± 3.9 vs end of test 4.9 ± 2.3 pmol. 1−1, P=0.03). During tilting, adrenocorticotrophic hormone, cortisol, and noradrenaline increased; 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 μg. kg −1. min −1 infusion), administered in a double-blind fashion during head-up tilt in nine subjects, failed tomodify 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.