Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs: Role of red blood cells

R. S. Sprague, A. H. Stephenson, R. A. Dimmitt, N. A. Weintraub, C. A. Branch, L. McMurdo, A. J. Lonigro

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Nitric oxide (NO) is produced by and relaxes pulmonary arteries and veins; however, a role for NO as a participant in the control of pulmonary vascular resistance (PVR) remains to be defined. Here we investigated the hypothesis that for NO to serve as a determinant of PVR in the rabbit requires the presence of blood. In isolated blood-perfused rabbit lungs, N(G)-nitro-L- arginine methyl ester (L-NAME, 100 μM) increased PVR and the slope of the pressure-flow relationship. These effects of L-NAME were prevented by pretreatment with L-arginine. In contrast, in lungs perfused with a physiological salt solution, L-NAME had no effect on PVR or the pressure flow relationship. The addition of washed red blood cells (RBCs) to physiological salt solution, but not the addition of plasma and platelets, restored the response to L-NAME. This effect of RBCs was not reproduced by increasing perfusate viscosity with dextran. These results suggest that, in the rabbit lung, NO is a determinant of PVR in the presence of blood. Moreover, that aspect of blood that permits the generation of NO appears to be related to the RBC and not to perfusate viscosity.

Original languageEnglish (US)
Pages (from-to)H1941-H1948
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume269
Issue number6 38-6
StatePublished - Dec 1 1995

Fingerprint

NG-Nitroarginine Methyl Ester
Vascular Resistance
Nitric Oxide
Erythrocytes
Rabbits
Pressure
Lung
Viscosity
Salts
Pulmonary Veins
Dextrans
Pulmonary Artery
Arginine
Blood Platelets

Keywords

  • L-arginine
  • prostacyclin
  • pulmonary vascular resistance
  • shear stress
  • transpulmonary pressure
  • viscosity

ASJC Scopus subject areas

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

Cite this

Sprague, R. S., Stephenson, A. H., Dimmitt, R. A., Weintraub, N. A., Branch, C. A., McMurdo, L., & Lonigro, A. J. (1995). Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs: Role of red blood cells. American Journal of Physiology - Heart and Circulatory Physiology, 269(6 38-6), H1941-H1948.

Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs : Role of red blood cells. / Sprague, R. S.; Stephenson, A. H.; Dimmitt, R. A.; Weintraub, N. A.; Branch, C. A.; McMurdo, L.; Lonigro, A. J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 269, No. 6 38-6, 01.12.1995, p. H1941-H1948.

Research output: Contribution to journalArticle

Sprague, RS, Stephenson, AH, Dimmitt, RA, Weintraub, NA, Branch, CA, McMurdo, L & Lonigro, AJ 1995, 'Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs: Role of red blood cells', American Journal of Physiology - Heart and Circulatory Physiology, vol. 269, no. 6 38-6, pp. H1941-H1948.
Sprague, R. S. ; Stephenson, A. H. ; Dimmitt, R. A. ; Weintraub, N. A. ; Branch, C. A. ; McMurdo, L. ; Lonigro, A. J. / Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs : Role of red blood cells. In: American Journal of Physiology - Heart and Circulatory Physiology. 1995 ; Vol. 269, No. 6 38-6. pp. H1941-H1948.
@article{18a03e0548714e30b21542dcdf77bdd2,
title = "Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs: Role of red blood cells",
abstract = "Nitric oxide (NO) is produced by and relaxes pulmonary arteries and veins; however, a role for NO as a participant in the control of pulmonary vascular resistance (PVR) remains to be defined. Here we investigated the hypothesis that for NO to serve as a determinant of PVR in the rabbit requires the presence of blood. In isolated blood-perfused rabbit lungs, N(G)-nitro-L- arginine methyl ester (L-NAME, 100 μM) increased PVR and the slope of the pressure-flow relationship. These effects of L-NAME were prevented by pretreatment with L-arginine. In contrast, in lungs perfused with a physiological salt solution, L-NAME had no effect on PVR or the pressure flow relationship. The addition of washed red blood cells (RBCs) to physiological salt solution, but not the addition of plasma and platelets, restored the response to L-NAME. This effect of RBCs was not reproduced by increasing perfusate viscosity with dextran. These results suggest that, in the rabbit lung, NO is a determinant of PVR in the presence of blood. Moreover, that aspect of blood that permits the generation of NO appears to be related to the RBC and not to perfusate viscosity.",
keywords = "L-arginine, prostacyclin, pulmonary vascular resistance, shear stress, transpulmonary pressure, viscosity",
author = "Sprague, {R. S.} and Stephenson, {A. H.} and Dimmitt, {R. A.} and Weintraub, {N. A.} and Branch, {C. A.} and L. McMurdo and Lonigro, {A. J.}",
year = "1995",
month = "12",
day = "1",
language = "English (US)",
volume = "269",
pages = "H1941--H1948",
journal = "American Journal of Physiology - Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "6 38-6",

}

TY - JOUR

T1 - Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs

T2 - Role of red blood cells

AU - Sprague, R. S.

AU - Stephenson, A. H.

AU - Dimmitt, R. A.

AU - Weintraub, N. A.

AU - Branch, C. A.

AU - McMurdo, L.

AU - Lonigro, A. J.

PY - 1995/12/1

Y1 - 1995/12/1

N2 - Nitric oxide (NO) is produced by and relaxes pulmonary arteries and veins; however, a role for NO as a participant in the control of pulmonary vascular resistance (PVR) remains to be defined. Here we investigated the hypothesis that for NO to serve as a determinant of PVR in the rabbit requires the presence of blood. In isolated blood-perfused rabbit lungs, N(G)-nitro-L- arginine methyl ester (L-NAME, 100 μM) increased PVR and the slope of the pressure-flow relationship. These effects of L-NAME were prevented by pretreatment with L-arginine. In contrast, in lungs perfused with a physiological salt solution, L-NAME had no effect on PVR or the pressure flow relationship. The addition of washed red blood cells (RBCs) to physiological salt solution, but not the addition of plasma and platelets, restored the response to L-NAME. This effect of RBCs was not reproduced by increasing perfusate viscosity with dextran. These results suggest that, in the rabbit lung, NO is a determinant of PVR in the presence of blood. Moreover, that aspect of blood that permits the generation of NO appears to be related to the RBC and not to perfusate viscosity.

AB - Nitric oxide (NO) is produced by and relaxes pulmonary arteries and veins; however, a role for NO as a participant in the control of pulmonary vascular resistance (PVR) remains to be defined. Here we investigated the hypothesis that for NO to serve as a determinant of PVR in the rabbit requires the presence of blood. In isolated blood-perfused rabbit lungs, N(G)-nitro-L- arginine methyl ester (L-NAME, 100 μM) increased PVR and the slope of the pressure-flow relationship. These effects of L-NAME were prevented by pretreatment with L-arginine. In contrast, in lungs perfused with a physiological salt solution, L-NAME had no effect on PVR or the pressure flow relationship. The addition of washed red blood cells (RBCs) to physiological salt solution, but not the addition of plasma and platelets, restored the response to L-NAME. This effect of RBCs was not reproduced by increasing perfusate viscosity with dextran. These results suggest that, in the rabbit lung, NO is a determinant of PVR in the presence of blood. Moreover, that aspect of blood that permits the generation of NO appears to be related to the RBC and not to perfusate viscosity.

KW - L-arginine

KW - prostacyclin

KW - pulmonary vascular resistance

KW - shear stress

KW - transpulmonary pressure

KW - viscosity

UR - http://www.scopus.com/inward/record.url?scp=0029558622&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029558622&partnerID=8YFLogxK

M3 - Article

C2 - 8594902

AN - SCOPUS:0029558622

VL - 269

SP - H1941-H1948

JO - American Journal of Physiology - Heart and Circulatory Physiology

JF - American Journal of Physiology - Heart and Circulatory Physiology

SN - 0363-6135

IS - 6 38-6

ER -