Perfusate viscosity and hematocrit determine pulmonary vascular responsiveness to no synthesis inhibitors. Wilson, Peter S., Pavel Khimenko, Timothy M. Moore, and Aubrey E. Taylor. Department of Physiology, University of South Alabama College of Medicine, Mobile, AL 36688
APStracts 2:0474H, 1995.
The pulmonary vascular responses to changes in perfusate viscosity were studied in isolated rat lungs treated with the nitric oxide synthesis (NOS) inhibitors, N_-nitro-L-arginine methyl ester (LNAME) and methyl L-arginine (LMA). Lungs were isolated according to standard protocols and perfused with varying concentrations of albumin in physiologic salt solution (PSS) and with low, intermediate, and normal hematocrits using washed erythrocytes. Pressure-flow curves were generated by increasing pulmonary artery pressure (PPA) while keeping pulmonary venous pressure (PPV) constant and measuring flow at each pressure interval. Neither perfusate flow nor pulmonary vascular resistance (PVR) changed after LNAME or LMA (300[mu]M) at any pressure interval in lungs perfused with 4% and 10% albumin/PSS. In lungs perfused with 20% albumin/PSS, LMA decreased flow at all PPA tested except 10 cm H2O (p&LT0.05). LNAME decreased flow in lungs perfused with normal (39.2 +/- 2.1%) hematocrits at all PPA tested. Conversely, LNAME decreased flow in lungs perfused with low and intermediate hematocrits only at the highest pressure intervals. L-arginine, when given after NOS inhibitors, failed to restore flow to baseline values in any group of lungs. DNAME (300[mu]M) did not change flow at any pressure interval in lungs perfused with normal (43 +/- 1.5%) hematocrit washed erythrocytes. We conclude that lungs perfused with intermediate- and normal-hematocrit washed erythrocytes, as well as with high- viscosity albumin/PSS solutions, show increased pulmonary vascular responses to NOS inhibitors.

Received 24 July 1995; accepted in final form 5 October 1995.
APS Manuscript Number H698-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95