Circulatory control mechanisms in vasodepressor syncope

Goldstein, David S.; Spanarkel, Marybeth; Pitterman, Arthur; Toltzis, Robert J.; Gratz, Edward; Epstein, Stephen E.; Keiser, Harry R.

doi:10.1016/0002-8703(82)90442-2

Cited by 102 publications

(42 citation statements)

References 7 publications

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“…This was then followed by progressive MSNA inhibition until complete disappearance and syncope. Attempts to evaluate sympathetic function with plasma NorEpi in neurally mediated syncope have produced variable and seemingly contradictory results; NorEpi concentrations have been reported to be either relatively low (13,26,27), normal (28), or moderately elevated (4,29,30). Confounding factors such as time of sampling, potential changes in NorEpi clearance, and alterations in spillover to the general circulation are likely to account for these contradictory results (17,31).…”

Section: Discussionmentioning

confidence: 99%

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

et al. 1997

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The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5 Ϯ 1 episodes/mo, n ϭ 14), age-and sex-matched controls (CON, n ϭ 23), and in healthy subjects who consistently experienced syncope during tilt (FS ϩ , n ϭ 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS ϩ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope. ( J. Clin. Invest. 1997. 99:2736-2744.)

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Section: Discussionmentioning

confidence: 99%

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

et al. 1997

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“…Even mild, asymptomatic hypoglycemia elicits larger increases in epinephrine than norepinephrine levels, and in the relatively benign form of circulatory failure represented by fainting, plasma epinephrine concentrations increase with smaller increases in plasma norepinephrine concentrations (Goldstein et al, 1982).…”

Section: Downloaded Frommentioning

confidence: 99%

Sources and Significance of Plasma Levels of Catechols and Their Metabolites in Humans

Goldstein¹,

Eisenhofer²,

Kopin³

2003

J Pharmacol Exp Ther

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377

322

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Human plasma contains several catechols, including the catecholamines norepinephrine, epinephrine, and dopamine, their precursor, L-3,4-dihydroxyphenylalanine (L-DOPA), and their deaminated metabolites, dihydroxyphenylglycol, the main neuronal metabolite of norepinephrine, and dihydroxyphenylacetic acid, a deaminated metabolite of dopamine. Products of metabolism of catechols include 3-methoxytyrosine (from L-DOPA), homovanillic acid and dopamine sulfate (from dopamine), normetanephrine, vanillylmandelic acid, and methoxyhydroxyphenylglycol (from norepinephrine), and metanephrine (from epinephrine). Plasma levels of catechols and their metabolites have related but distinct sources and therefore reflect different functions of catecholamine systems. This article provides an update about plasma levels of catechols and their metabolites and the relevance of those levels to some issues in human health and disease.Near the end of the 19th century, soon after the description of the profound cardiovascular effects of injected adrenal extract and the purification and identification of epinephrine as the vasoactive principal of the adrenal gland, researchers began to develop chemical means to assess activity of what came to be called the sympathoadrenomedullary system. The first chemical method for such measurement was colorimetric, based on the unusual susceptibility of epinephrine to oxidize, forming a brownish compound called "adrenochrome". Early attempts to measure circulating levels of epinephrine and related compounds chemically failed, mainly because the potency of epinephrine corresponds to very low normal concentrations in the bloodstream. Bioassays such as used by the great American physiologist, Walter B. Cannon were the first to detect successfully epinephrine release into the circulation. Cannon later developed and exploited a preparation based on the magnitude of the increase in heart rate in animals with denervated hearts; abolition of the increase by adrenalectomy confirmed the hormone's adrenal source. Subsequent chemical methods depended on fluorescence detection (after the trihydroxyindole reaction or ethylenediamine condensation) or radioenzymatic assays (after methylation with S-adenosylmethionine and catechol-Omethyltransferase). Ironically, current sensitive chemical methods using liquid chromatography with electrochemical detection depend on the same catechol oxidation as did the original colorimetric method.For almost the whole of the first half of the last century, epinephrine was the only catecholamine to receive attention. Cannon proposed-erroneously-that epinephrine was not only the main vasoactive hormone released by the adrenal gland but also the chemical messenger released from sympathetic nerves. This fit with his concept of a unitary sympathoadrenomedullary system, which would help maintain homeostasis (a word he coined) during emergencies but would not be necessary in day-to-day life. Fifty years after the discovery of epinephrine, norepinephrine, rather than epinephrine, was fi...

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“…Microneurographic studies have shown that precipitously decreased skeletal sym pathetic nervous outflow accompanies the vaso dilation [5]. Plasma noradrenaline (NA) levels, measured immediately after or at the time of fainting, are decreased or inappropriately normal [6,7] and release of NA into the venous drainage in the heart [8] and kidneys [9] decreases virtually to zero. In contrast, plasma adrenaline (A) levels often are increased [6].…”

Section: Introductionmentioning

confidence: 99%

“…Plasma noradrenaline (NA) levels, measured immediately after or at the time of fainting, are decreased or inappropriately normal [6,7] and release of NA into the venous drainage in the heart [8] and kidneys [9] decreases virtually to zero. In contrast, plasma adrenaline (A) levels often are increased [6]. Vagal bradycardia does riot cause vaso depressor reactions, because parasympatholytic drugs may not reverse or prevent the hypotension [10].…”

Section: Introductionmentioning

confidence: 99%

Neurohumoral antecedents of vasodepressor reactions

Jacobs

Goldstein²,

Willemsen

et al. 1995

Eur J Clin Investigation

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Abstract. 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 condi tions for this dramatic syndrome are poorly under stood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently devel oped 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 -4 0 mmHg 11 subjects had vasodepressor reac tions, with sudden hypotension, nausea, and dizzi ness. 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 -15mmHg (A^-0*06± (S E M ) 0*04pmol m in'1100 mL" 1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (A = 0*31 ±0* 13 pmol m in '1 lOOmL" 1). Plasma levels of /?-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40 mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinbibition, and release of endogenous opioids can precede vasode pressor syncope.

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Circulatory control mechanisms in vasodepressor syncope

Cited by 102 publications

References 7 publications

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

Sources and Significance of Plasma Levels of Catechols and Their Metabolites in Humans

Neurohumoral antecedents of vasodepressor reactions

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