Effect of l-name on pressure-flow relationships in isolated rabbit
lungs: role of red blood cells.
Sprague, Randy S., Alan H. Stephenson, Reed A. Dimmitt, Neal A.
Weintraub, Carrie A. Branch, Lorraine McMurdo, and Andrew J. Lonigro.
Departments of Medicine and Pharmacological and Physiological
Science, Saint Louis University School of Medicine, St. Louis,
Missouri 63104
APStracts 2:0244H, 1995.
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, NG-nitro-L-arginine methyl ester (L-NAME, 100
[mu]M) increased both 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 (PSS), L-NAME had no effect on either PVR or the
pressure-flow relationship. The addition of washed red blood cells
(RBCs) to PSS, 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 which permits the generation
of NO appears to be related to the RBC and not to perfusate
viscosity.
Received 13 March 1995; accepted in final form 2 June 1995.
APS Manuscript Number H238-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.