beta-endorphin has been researched along with Syncope* in 6 studies
6 other study(ies) available for beta-endorphin and Syncope
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Endogenous opioids and epinephrine in nitroglycerin provocation tilt test in patients with neurally mediated syncope.
Endogenous opioids and catecholamines are involved in autonomic activity. Nitroglycerin provocation tilt is a useful modality for evaluating neurally mediated syncope. Endogenous opioids and epinephrine might play an important role in nitroglycerin provocation tilt. To investigate whether or not opioids and catecholamines are involved in the pathogenesis of nitroglycerin provocation tilt, we measured the temporal changes of the plasma levels of beta endorphin, norepinephrine, and epinephrine in 64 patients with syncope of unknown etiology, and compared the findings with those of 16 patients who underwent isoproterenol provocation tilt (1-3 microg/min) test with a positive response. We performed a 20 minute control tilt (80 degrees) followed by a nitroglycerin provocation tilt of 20 minutes with the intravenous infusion of nitroglycerin. Nitroglycerin infusion was started at 250 microg/h, and was increased by 250 microg/h every 3 minutes up to 1500 microg/h during the tilt test. Beta-endorphin, norepinephrine, and epinephrine were measured in peripheral venous blood in the supine position 2, 10, and 20 minutes after the start of the tilt test, and also at the onset of syncope. Twenty-six patients had a positive response to the control tilt (group 1), and 22 patients had a positive response to nitroglycerin provocation tilt (group 2). The remaining 16 patients had a negative response to both control tilt and nitroglycerin provocation tilt (group 3), compared with isoproterenol provocation tilt patients (group 4). Beta-endorphin and epinephrine only significantly increased in groups 1 and 2 (beta-endorphin; from 7.3 +/- 3.3 pg/mL to 19.9 +/- 17.7 pg/mL, in group 1, P < 0.05; from 7.3 +/- 2.9 to 16.5 +/- 10.7 pg/mL, in group 2, P < 0.05; epinephrine; from 42 +/- 58 pg/mL to 157 +/- 161 pg/mL, in group 1, P < 0.05: from 33 +/- 25 to 202 +/- 252 pg/mL, in group 2, P < 0.05), but not in groups 3 and 4. Beta-endorphin and epinephrine might participate in the pathophysiology in conventional tilt-induced as well as nitroglycerin provocation tilt-induced syncope in patients with neurally mediated syncope. Topics: Adolescent; Adult; Aged; Analysis of Variance; beta-Endorphin; Blood Pressure; Epinephrine; Female; Heart Rate; Humans; Isoproterenol; Male; Middle Aged; Nitroglycerin; Norepinephrine; Opioid Peptides; Syncope; Tilt-Table Test | 2003 |
Increase in plasma beta endorphins precedes vasodepressor syncope.
Topics: Angiotensin-Converting Enzyme Inhibitors; beta-Endorphin; Humans; Hypotension; Syncope | 1995 |
Neurohumoral antecedents of vasodepressor reactions.
Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine conditions for this dramatic syndrome are poorly understood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently developed vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40 mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -40 mmHg 11 subjects had vasodepressor reactions, with sudden hypotension, nausea, and dizziness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15 mmHg (delta = -0.06 +/- (SEM) 0.04 pmol min-1 100mL-1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (delta = 0.31 +/- 0.13 pmol min-1 100mL-1). Plasma levels of beta-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinhibition, and release of endogenous opioids can precede vasodepressor syncope. Topics: beta-Endorphin; Hemodynamics; Humans; Lower Body Negative Pressure; Male; Norepinephrine; Syncope; Time Factors | 1995 |
Increase in plasma beta endorphins precedes vasodepressor syncope.
Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting.. To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope.. 24 patients undergoing tilt testing for investigation of unexplained syncope.. Tertiary referral centre.. Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l).. Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)).. An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids. Topics: Adolescent; Adult; Aged; beta-Endorphin; Female; Humans; Male; Middle Aged; Posture; Reproducibility of Results; Syncope; Vasomotor System | 1994 |
Increase in plasma beta endorphins precedes vasodepressor syncope.
Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting.. To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope.. 24 patients undergoing tilt testing for investigation of unexplained syncope.. Tertiary referral centre.. Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l).. Patients with a positive test showed a rise in beta endorphin concentrations before syncope (baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)).. An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids. Topics: Adolescent; Adult; Aged; beta-Endorphin; Female; Humans; Hypotension; Male; Middle Aged; Posture; Radioimmunoassay; Reproducibility of Results; Syncope; Vascular Resistance | 1994 |
Increase of plasma beta endorphins in vasodepressor syncope.
Topics: Adolescent; Adult; beta-Endorphin; Child; Female; Humans; Male; Syncope | 1990 |