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 journalArticlepeer-review

65 Scopus citations


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
Issue number6 38-6
StatePublished - 1995
Externally publishedYes


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

ASJC Scopus subject areas

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


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