Hemoglobin and red cells alter the response of expired nitric oxide to mechanical forces.
Berg, John T., Steven Deem, Mark E. Kerr, and Erik R. Swenson.
Departments of Medicine and Anesthesiology, Veterans Affairs Puget Sound Health Care System and
the University of Washington, Seattle, Washington 98108
APStracts 7:0469H, 2000.
Expired nitric oxide (NOe) varies with hemodynamic or ventilatory perturbations, possibly due to shear
stress- or stretch-stimulated NO production. Since hemoglobin (Hb) binds NO, NOe changes may reflect
changes in blood volume and flow. To determine the role of blood and mechanical forces, we measured
NOe in anesthetized rabbits, as well as rabbit lungs perfused with buffer, red blood cells (RBCs) or Hb
following changes in flow, venous pressure (Pv), and positive end-expiratory pressure (PEEP). In buffer-
perfused lungs decreases in flow and Pv reduced NOe, but NOe rose when RBCs and Hb were present.
These findings are consistent with changes in vascular NO production, whose detection is obscured in
blood-perfused lungs by the more dominant effect of Hb NO scavenging. PEEP decreased NOe in all
perfused lungs but increased NOe in live rabbits. The NOe fall with PEEP in isolated lungs is consistent
with flow redistribution from alveolar septal capillaries to extra-alveolar vessels and decreased surface area
or a direct, stretch-mediated depression of lung epithelial NO production. In live rabbits, increased NOe
may reflect blood flow reduction and decreased Hb NO scavenging and/or autonomic responses that
increase NO production. We conclude that blood and systemic responses render it difficult to use NOe
changes as an accurate measure of lung tissue NO production.
Received 24 February 2000; accepted in final form 27 July 2000
APS Manuscript Number H168-0.
Article publication pending Am J Physiol Heart Circ Physiol
ISSN 1080-4757 Copyright 2000 The American Physiological Society.
Published in APStracts on 20 October 2000