RED-BLOOD-CELL AUGMENTATION OF HYPOXIC PULMONARY VASOCONSTRICTION - HEMATOCRIT DEPENDENCE AND THE IMPORTANCE OF NITRIC-OXIDE

Red blood cells (RBCs) are known to augment hypoxic pulmonary vasocons triction (HPV). To determine whether this phenomenon is hematocrit (Hc t) dependent and related to alterations of either nitric oxide (NO) or adenosine metabolism, we studied mechanically ventilated, pump-perfus ed lungs from euthanized New Zealand White rabbits. Lungs were perfuse d in situ in a recirculating manner at constant flow; perfusates consi sted of Krebs-Henseleit buffer or buffer plus washed RBCs at a Hct of 10% or 30%. HPV was quantitated as the increase in pulmonary artery pr essure (Ppa) from baseline after 5 min of hypoxia. In three experiment al sets, we studied the effects of Hct on HPV and expired NO, the effe cts of nitric oxide synthase (NOS) inhibition, and the effects of aden osine receptor blockade. HPV was greater at a higher Hct, and expired NO varied inversely with Hct and decreased with hypoxia. NOS inhibitio n eliminated RBC-dependence of HPV. Adenosine-receptor blockade did no t affect the RBC-dependence of HPV. We conclude that HPV is dependent on Hct, and that this phenomenon may be related to scavenging of NO bu t not adenosine by RBCs.