Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

Background. Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin- aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably 'asymptomatic' ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise. Methods and Results. ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48±2 to 29±4%), cardiac output (4.64±0.29 to 2.89±0.17 L/min), and mean arterial pressure (119±4 to 108±4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60±19 to 165±27 pg/mL) and norepinephrine (382±127 to 690±211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V̇) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V̇ similar to that observed with volume expansion before producing ALVD. Conclusions. The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.

Original languageEnglish (US)
Pages (from-to)2016-2022
Number of pages7
JournalCirculation
Volume87
Issue number6
StatePublished - 1993

Fingerprint

Left Ventricular Dysfunction
Canidae
Ventricular Dysfunction
Atrial Natriuretic Factor
Renin-Angiotensin System
Kidney
Norepinephrine
Hemodynamics
Sodium
Atrial Pressure
Vasoconstriction
Cardiac Output
Vascular Resistance
Creatinine
Arterial Pressure
Dogs

Keywords

  • atrial natriuretic factor
  • congestive heart failure
  • hemodynamics
  • renal function

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction. / Redfield, Margaret May; Aarhus, L. L.; Wright, R. Scott; Burnett, John C Jr.

In: Circulation, Vol. 87, No. 6, 1993, p. 2016-2022.

Research output: Contribution to journalArticle

@article{d3bb44d8238a48e7ad3c51988464e800,
title = "Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction",
abstract = "Background. Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin- aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably 'asymptomatic' ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise. Methods and Results. ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48±2 to 29±4{\%}), cardiac output (4.64±0.29 to 2.89±0.17 L/min), and mean arterial pressure (119±4 to 108±4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60±19 to 165±27 pg/mL) and norepinephrine (382±127 to 690±211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V̇) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V̇ similar to that observed with volume expansion before producing ALVD. Conclusions. The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.",
keywords = "atrial natriuretic factor, congestive heart failure, hemodynamics, renal function",
author = "Redfield, {Margaret May} and Aarhus, {L. L.} and Wright, {R. Scott} and Burnett, {John C Jr.}",
year = "1993",
language = "English (US)",
volume = "87",
pages = "2016--2022",
journal = "Circulation",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction

AU - Redfield, Margaret May

AU - Aarhus, L. L.

AU - Wright, R. Scott

AU - Burnett, John C Jr.

PY - 1993

Y1 - 1993

N2 - Background. Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin- aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably 'asymptomatic' ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise. Methods and Results. ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48±2 to 29±4%), cardiac output (4.64±0.29 to 2.89±0.17 L/min), and mean arterial pressure (119±4 to 108±4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60±19 to 165±27 pg/mL) and norepinephrine (382±127 to 690±211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V̇) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V̇ similar to that observed with volume expansion before producing ALVD. Conclusions. The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.

AB - Background. Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin- aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably 'asymptomatic' ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise. Methods and Results. ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48±2 to 29±4%), cardiac output (4.64±0.29 to 2.89±0.17 L/min), and mean arterial pressure (119±4 to 108±4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60±19 to 165±27 pg/mL) and norepinephrine (382±127 to 690±211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V̇) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V̇ similar to that observed with volume expansion before producing ALVD. Conclusions. The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.

KW - atrial natriuretic factor

KW - congestive heart failure

KW - hemodynamics

KW - renal function

UR - http://www.scopus.com/inward/record.url?scp=0027156408&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027156408&partnerID=8YFLogxK

M3 - Article

C2 - 8504516

AN - SCOPUS:0027156408

VL - 87

SP - 2016

EP - 2022

JO - Circulation

JF - Circulation

SN - 0009-7322

IS - 6

ER -