Beta-2 adrenoceptor control of the venous circulation in intact dogs

R. W. Lee, T. E. Raya, R. G. Gay, M. Olajos, Steven Goldman

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The effects of beta-2 adrenoceptor stimulation on the peripheral circulation in 10 dogs were evaluated. All studies were done during ganglion blockade with hexamethonium. Venous capacitance was assessed by measuring mean circulatory filling pressure, venous compliance and unstressed vascular volume. Beta-2 stimulation was achieved with terbutaline (27 μg/min) after beta-1 blockade with metoprolol (0.75 mg/kg). At a dose of terbutaline that decreased mean aortic pressure from 80.4 ± 3.5 to 58.9 ± 1.9 mm Hg (p < .01), there was no change in cardiac index (155.8 ± 10.5 vs. 161.1 ±9.1 ml/kg/min) despite an increase in heart rate from 118.6 ± 5.2 to 132.6 ± 5.0 beats/min. Right atrial pressure, left ventricular end-diastolic pressure and dP/dt did not change. Systemic vascular resistance decreased from 0.52 ± 0.02 to 0.39 ± 0.03 mm Hg·min·kg·ml (P < .01). Arterial compliance increased from 0.067 ± 0.003 to 0.088 ± 0.007 ml/mm Hg/kg and the volume of blood shifted out of the larger arteries was 1.8 ± 0.4 ml/kg. Mean circulatory filling pressure did not change but venous compliance decreased from 1.90 ± 0.04 to 1.47 ± 0.06 ml/mm Hg/kg and unstressed vascular volume increased from -14.5 ± 0.5 to -8.4 ± 0.5 ml/kg. Central blood volume increased from 22.8 ± 1.1 to 27.4 ± 2.2 ml/kg. There was an increase in total blood volume from 81.1 ± 2.7 to 90.5 ± 3.7 ml/kg. To determine the extent to which changes in the spleen were responsible for these observations, five dogs were studied 2 weeks after splenectomy. Base-line hemodynamics were unchanged and beta-2 stimulation in the splenectomized dogs resulted in a decrease in venous compliance with no changes in arterial compliance, total blood volume or unstressed vascular volume. In summary, specific beta-2 adrenoceptor stimulation results in a decrease in venous compliance and volume shifts into the central compartment and out of the arterial system. The results suggest that three changes represent direct effects of beta 2 adrenoceptor stimulation on the systemic venous circulation.

Original languageEnglish (US)
Pages (from-to)1138-1143
Number of pages6
JournalJournal of Pharmacology and Experimental Therapeutics
Volume242
Issue number3
StatePublished - 1987

Fingerprint

Adrenergic Receptors
Compliance
Blood Volume
Dogs
Blood Vessels
Terbutaline
Hexamethonium
Metoprolol
Venous Pressure
Atrial Pressure
Splenectomy
Ganglia
Vascular Resistance
Arterial Pressure
Spleen
Arteries
Heart Rate
Hemodynamics
Blood Pressure
Pressure

ASJC Scopus subject areas

  • Pharmacology

Cite this

Beta-2 adrenoceptor control of the venous circulation in intact dogs. / Lee, R. W.; Raya, T. E.; Gay, R. G.; Olajos, M.; Goldman, Steven.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 242, No. 3, 1987, p. 1138-1143.

Research output: Contribution to journalArticle

Lee, R. W. ; Raya, T. E. ; Gay, R. G. ; Olajos, M. ; Goldman, Steven. / Beta-2 adrenoceptor control of the venous circulation in intact dogs. In: Journal of Pharmacology and Experimental Therapeutics. 1987 ; Vol. 242, No. 3. pp. 1138-1143.
@article{cfd8b8b05f884c50a62e662056aa54cd,
title = "Beta-2 adrenoceptor control of the venous circulation in intact dogs",
abstract = "The effects of beta-2 adrenoceptor stimulation on the peripheral circulation in 10 dogs were evaluated. All studies were done during ganglion blockade with hexamethonium. Venous capacitance was assessed by measuring mean circulatory filling pressure, venous compliance and unstressed vascular volume. Beta-2 stimulation was achieved with terbutaline (27 μg/min) after beta-1 blockade with metoprolol (0.75 mg/kg). At a dose of terbutaline that decreased mean aortic pressure from 80.4 ± 3.5 to 58.9 ± 1.9 mm Hg (p < .01), there was no change in cardiac index (155.8 ± 10.5 vs. 161.1 ±9.1 ml/kg/min) despite an increase in heart rate from 118.6 ± 5.2 to 132.6 ± 5.0 beats/min. Right atrial pressure, left ventricular end-diastolic pressure and dP/dt did not change. Systemic vascular resistance decreased from 0.52 ± 0.02 to 0.39 ± 0.03 mm Hg·min·kg·ml (P < .01). Arterial compliance increased from 0.067 ± 0.003 to 0.088 ± 0.007 ml/mm Hg/kg and the volume of blood shifted out of the larger arteries was 1.8 ± 0.4 ml/kg. Mean circulatory filling pressure did not change but venous compliance decreased from 1.90 ± 0.04 to 1.47 ± 0.06 ml/mm Hg/kg and unstressed vascular volume increased from -14.5 ± 0.5 to -8.4 ± 0.5 ml/kg. Central blood volume increased from 22.8 ± 1.1 to 27.4 ± 2.2 ml/kg. There was an increase in total blood volume from 81.1 ± 2.7 to 90.5 ± 3.7 ml/kg. To determine the extent to which changes in the spleen were responsible for these observations, five dogs were studied 2 weeks after splenectomy. Base-line hemodynamics were unchanged and beta-2 stimulation in the splenectomized dogs resulted in a decrease in venous compliance with no changes in arterial compliance, total blood volume or unstressed vascular volume. In summary, specific beta-2 adrenoceptor stimulation results in a decrease in venous compliance and volume shifts into the central compartment and out of the arterial system. The results suggest that three changes represent direct effects of beta 2 adrenoceptor stimulation on the systemic venous circulation.",
author = "Lee, {R. W.} and Raya, {T. E.} and Gay, {R. G.} and M. Olajos and Steven Goldman",
year = "1987",
language = "English (US)",
volume = "242",
pages = "1138--1143",
journal = "Journal of Pharmacology and Experimental Therapeutics",
issn = "0022-3565",
publisher = "American Society for Pharmacology and Experimental Therapeutics",
number = "3",

}

TY - JOUR

T1 - Beta-2 adrenoceptor control of the venous circulation in intact dogs

AU - Lee, R. W.

AU - Raya, T. E.

AU - Gay, R. G.

AU - Olajos, M.

AU - Goldman, Steven

PY - 1987

Y1 - 1987

N2 - The effects of beta-2 adrenoceptor stimulation on the peripheral circulation in 10 dogs were evaluated. All studies were done during ganglion blockade with hexamethonium. Venous capacitance was assessed by measuring mean circulatory filling pressure, venous compliance and unstressed vascular volume. Beta-2 stimulation was achieved with terbutaline (27 μg/min) after beta-1 blockade with metoprolol (0.75 mg/kg). At a dose of terbutaline that decreased mean aortic pressure from 80.4 ± 3.5 to 58.9 ± 1.9 mm Hg (p < .01), there was no change in cardiac index (155.8 ± 10.5 vs. 161.1 ±9.1 ml/kg/min) despite an increase in heart rate from 118.6 ± 5.2 to 132.6 ± 5.0 beats/min. Right atrial pressure, left ventricular end-diastolic pressure and dP/dt did not change. Systemic vascular resistance decreased from 0.52 ± 0.02 to 0.39 ± 0.03 mm Hg·min·kg·ml (P < .01). Arterial compliance increased from 0.067 ± 0.003 to 0.088 ± 0.007 ml/mm Hg/kg and the volume of blood shifted out of the larger arteries was 1.8 ± 0.4 ml/kg. Mean circulatory filling pressure did not change but venous compliance decreased from 1.90 ± 0.04 to 1.47 ± 0.06 ml/mm Hg/kg and unstressed vascular volume increased from -14.5 ± 0.5 to -8.4 ± 0.5 ml/kg. Central blood volume increased from 22.8 ± 1.1 to 27.4 ± 2.2 ml/kg. There was an increase in total blood volume from 81.1 ± 2.7 to 90.5 ± 3.7 ml/kg. To determine the extent to which changes in the spleen were responsible for these observations, five dogs were studied 2 weeks after splenectomy. Base-line hemodynamics were unchanged and beta-2 stimulation in the splenectomized dogs resulted in a decrease in venous compliance with no changes in arterial compliance, total blood volume or unstressed vascular volume. In summary, specific beta-2 adrenoceptor stimulation results in a decrease in venous compliance and volume shifts into the central compartment and out of the arterial system. The results suggest that three changes represent direct effects of beta 2 adrenoceptor stimulation on the systemic venous circulation.

AB - The effects of beta-2 adrenoceptor stimulation on the peripheral circulation in 10 dogs were evaluated. All studies were done during ganglion blockade with hexamethonium. Venous capacitance was assessed by measuring mean circulatory filling pressure, venous compliance and unstressed vascular volume. Beta-2 stimulation was achieved with terbutaline (27 μg/min) after beta-1 blockade with metoprolol (0.75 mg/kg). At a dose of terbutaline that decreased mean aortic pressure from 80.4 ± 3.5 to 58.9 ± 1.9 mm Hg (p < .01), there was no change in cardiac index (155.8 ± 10.5 vs. 161.1 ±9.1 ml/kg/min) despite an increase in heart rate from 118.6 ± 5.2 to 132.6 ± 5.0 beats/min. Right atrial pressure, left ventricular end-diastolic pressure and dP/dt did not change. Systemic vascular resistance decreased from 0.52 ± 0.02 to 0.39 ± 0.03 mm Hg·min·kg·ml (P < .01). Arterial compliance increased from 0.067 ± 0.003 to 0.088 ± 0.007 ml/mm Hg/kg and the volume of blood shifted out of the larger arteries was 1.8 ± 0.4 ml/kg. Mean circulatory filling pressure did not change but venous compliance decreased from 1.90 ± 0.04 to 1.47 ± 0.06 ml/mm Hg/kg and unstressed vascular volume increased from -14.5 ± 0.5 to -8.4 ± 0.5 ml/kg. Central blood volume increased from 22.8 ± 1.1 to 27.4 ± 2.2 ml/kg. There was an increase in total blood volume from 81.1 ± 2.7 to 90.5 ± 3.7 ml/kg. To determine the extent to which changes in the spleen were responsible for these observations, five dogs were studied 2 weeks after splenectomy. Base-line hemodynamics were unchanged and beta-2 stimulation in the splenectomized dogs resulted in a decrease in venous compliance with no changes in arterial compliance, total blood volume or unstressed vascular volume. In summary, specific beta-2 adrenoceptor stimulation results in a decrease in venous compliance and volume shifts into the central compartment and out of the arterial system. The results suggest that three changes represent direct effects of beta 2 adrenoceptor stimulation on the systemic venous circulation.

UR - http://www.scopus.com/inward/record.url?scp=0023205602&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023205602&partnerID=8YFLogxK

M3 - Article

C2 - 2821225

AN - SCOPUS:0023205602

VL - 242

SP - 1138

EP - 1143

JO - Journal of Pharmacology and Experimental Therapeutics

JF - Journal of Pharmacology and Experimental Therapeutics

SN - 0022-3565

IS - 3

ER -