Hemoglobin and red blood cells alter the response of expired nitric oxide to mechanical forces

• Published in: American journal of physiology. Heart and circulatory physiology 2000-12, Vol.279 (6), p.H2947-H2953
• Main Authors: Berg, John T, Deem, Steven, Kerr, Mark E, Swenson, Erik R
• Format: Article
• Language: English
• Subjects: Animals; Capillaries - physiology; Erythrocytes - physiology; Hematocrit; Hemoglobins - metabolism; In Vitro Techniques; Nitric Oxide - metabolism; Perfusion; Positive-Pressure Respiration; Pulmonary Alveoli - blood supply; Pulmonary Alveoli - physiology; Pulmonary Circulation - physiology; Pulmonary Wedge Pressure - physiology; Rabbits; Respiratory Mucosa - metabolism; Space life sciences; Stress, Mechanical
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.2000.279.6.h2947

Departments of Medicine and Anesthesiology, Veterans Affairs Puget Sound Health Care System and the University of Washington, Seattle, Washington 98108 Expired nitric oxide (NO e ) varies with hemodynamic or ventilatory perturbations, possibly due to shear stress- or stretch-stimulated NO production. Since hemoglobin (Hb) binds NO, NO e changes may reflect changes in blood volume and flow. To determine the role of blood and mechanical forces, we measured NO e in anesthetized rabbits, as well as rabbit lungs perfused with buffer, red blood cells (RBCs) or Hb following changes in flow, venous pressure (P v ), and positive end-expiratory pressure (PEEP). In buffer-perfused lungs decreases in flow and P v reduced NO e , but NO e 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 NO e in all perfused lungs but increased NO e in live rabbits. The NO e 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 NO e 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 NO e changes as an accurate measure of lung tissue NO production. shear stress; pulmonary circulation; positive end-expiratory pressure; pulmonary blood flow; pulmonary venous pressure