Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

Qi Fu, Shigeki Shibata, Jeffrey L Hastings, Anand Prasad, M. Dean Palmer, Benjamin D Levine

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Low levels (i.e., ≤20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload "selectively" cardiopulmonary baroreceptors in humans, since steady- state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20-54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan- Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and -15- and -30-mmHg LBNP for 6 min each. Application of - 15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after ∼15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at -5- and in all at - 10-mmHg LBNP. The delay for left ventricular stroke volume to fall at - 15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during - 15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at - 30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., - 10 and -15 mmHg) of LBNP in humans. Thus "selective" unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume296
Issue number2
DOIs
StatePublished - Feb 2009

Fingerprint

Lower Body Negative Pressure
Pressoreceptors
Blood Pressure
Heart Rate
Pulmonary Wedge Pressure
Atrial Pressure
Baroreflex
Stroke Volume
Pulmonary Artery
Hemodynamics
Cardiac Volume
Cardiac Output
Vascular Resistance
Reflex

Keywords

  • Arterial pressure
  • Baroreflexes
  • Hemodynamics

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Cite this

@article{ec30fcbdf4ad47dfb338e23fd8c2a59e,
title = "Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans",
abstract = "Low levels (i.e., ≤20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload {"}selectively{"} cardiopulmonary baroreceptors in humans, since steady- state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20-54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan- Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and -15- and -30-mmHg LBNP for 6 min each. Application of - 15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after ∼15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at -5- and in all at - 10-mmHg LBNP. The delay for left ventricular stroke volume to fall at - 15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during - 15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at - 30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., - 10 and -15 mmHg) of LBNP in humans. Thus {"}selective{"} unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.",
keywords = "Arterial pressure, Baroreflexes, Hemodynamics",
author = "Qi Fu and Shigeki Shibata and Hastings, {Jeffrey L} and Anand Prasad and Palmer, {M. Dean} and Levine, {Benjamin D}",
year = "2009",
month = "2",
doi = "10.1152/ajpheart.00184.2008",
language = "English (US)",
volume = "296",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

AU - Fu, Qi

AU - Shibata, Shigeki

AU - Hastings, Jeffrey L

AU - Prasad, Anand

AU - Palmer, M. Dean

AU - Levine, Benjamin D

PY - 2009/2

Y1 - 2009/2

N2 - Low levels (i.e., ≤20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload "selectively" cardiopulmonary baroreceptors in humans, since steady- state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20-54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan- Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and -15- and -30-mmHg LBNP for 6 min each. Application of - 15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after ∼15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at -5- and in all at - 10-mmHg LBNP. The delay for left ventricular stroke volume to fall at - 15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during - 15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at - 30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., - 10 and -15 mmHg) of LBNP in humans. Thus "selective" unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.

AB - Low levels (i.e., ≤20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload "selectively" cardiopulmonary baroreceptors in humans, since steady- state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20-54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan- Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and -15- and -30-mmHg LBNP for 6 min each. Application of - 15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after ∼15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at -5- and in all at - 10-mmHg LBNP. The delay for left ventricular stroke volume to fall at - 15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during - 15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at - 30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., - 10 and -15 mmHg) of LBNP in humans. Thus "selective" unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.

KW - Arterial pressure

KW - Baroreflexes

KW - Hemodynamics

UR - http://www.scopus.com/inward/record.url?scp=61949235609&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=61949235609&partnerID=8YFLogxK

U2 - 10.1152/ajpheart.00184.2008

DO - 10.1152/ajpheart.00184.2008

M3 - Article

VL - 296

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 2

ER -