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

Rogelio Mosqueda-Garcia, Raffaello Furlan, Roxana Fernandez-Violante, Tushar Desai, Marie Snell, Zoltan Jarai, Vasu Ananthram, Rose Marie Robertson, David Robertson

Research output: Contribution to journalArticle

Abstract

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±1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 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+ 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.

Original languageEnglish
Pages (from-to)2736-2744
Number of pages9
JournalJournal of Clinical Investigation
Volume99
Issue number11
Publication statusPublished - Jun 1 1997

Fingerprint

Baroreflex
Syncope
Muscles
Central Venous Pressure
Heart Rate
Blood Pressure
Hypovolemia
Nitroprusside
Phenylephrine
Bradycardia
Hypotension
Catecholamines
Norepinephrine
Healthy Volunteers
Hemodynamics

Keywords

  • Baroreflex
  • Microneurography
  • Neurocardiogenic syncope
  • Tilt
  • Vasovagal

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Mosqueda-Garcia, R., Furlan, R., Fernandez-Violante, R., Desai, T., Snell, M., Jarai, Z., ... Robertson, D. (1997). Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt. Journal of Clinical Investigation, 99(11), 2736-2744.

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt. / Mosqueda-Garcia, Rogelio; Furlan, Raffaello; Fernandez-Violante, Roxana; Desai, Tushar; Snell, Marie; Jarai, Zoltan; Ananthram, Vasu; Robertson, Rose Marie; Robertson, David.

In: Journal of Clinical Investigation, Vol. 99, No. 11, 01.06.1997, p. 2736-2744.

Research output: Contribution to journalArticle

Mosqueda-Garcia, R, Furlan, R, Fernandez-Violante, R, Desai, T, Snell, M, Jarai, Z, Ananthram, V, Robertson, RM & Robertson, D 1997, 'Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt', Journal of Clinical Investigation, vol. 99, no. 11, pp. 2736-2744.
Mosqueda-Garcia R, Furlan R, Fernandez-Violante R, Desai T, Snell M, Jarai Z et al. Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt. Journal of Clinical Investigation. 1997 Jun 1;99(11):2736-2744.
Mosqueda-Garcia, Rogelio ; Furlan, Raffaello ; Fernandez-Violante, Roxana ; Desai, Tushar ; Snell, Marie ; Jarai, Zoltan ; Ananthram, Vasu ; Robertson, Rose Marie ; Robertson, David. / Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt. In: Journal of Clinical Investigation. 1997 ; Vol. 99, No. 11. pp. 2736-2744.
@article{845cf56b6c5a469a95a23537e0198e3c,
title = "Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt",
abstract = "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±1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 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+ 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.",
keywords = "Baroreflex, Microneurography, Neurocardiogenic syncope, Tilt, Vasovagal",
author = "Rogelio Mosqueda-Garcia and Raffaello Furlan and Roxana Fernandez-Violante and Tushar Desai and Marie Snell and Zoltan Jarai and Vasu Ananthram and Robertson, {Rose Marie} and David Robertson",
year = "1997",
month = "6",
day = "1",
language = "English",
volume = "99",
pages = "2736--2744",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "11",

}

TY - JOUR

T1 - Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt

AU - Mosqueda-Garcia, Rogelio

AU - Furlan, Raffaello

AU - Fernandez-Violante, Roxana

AU - Desai, Tushar

AU - Snell, Marie

AU - Jarai, Zoltan

AU - Ananthram, Vasu

AU - Robertson, Rose Marie

AU - Robertson, David

PY - 1997/6/1

Y1 - 1997/6/1

N2 - 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±1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 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+ 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.

AB - 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±1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 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+ 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.

KW - Baroreflex

KW - Microneurography

KW - Neurocardiogenic syncope

KW - Tilt

KW - Vasovagal

UR - http://www.scopus.com/inward/record.url?scp=0031000274&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031000274&partnerID=8YFLogxK

M3 - Article

C2 - 9169504

AN - SCOPUS:0031000274

VL - 99

SP - 2736

EP - 2744

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 11

ER -