Nitric oxide and cgmp do not affect fluid flux in isolated rat lungs . Eichinger, Mark R., and Benjimen R. Walker. Department of Physiology, University of New Mexico, School of Medicine, Albuquerque, NM 87131
APStracts 2:0368A, 1995.
We sought to examine the influence of NO and the second messengers cGMP and intracellular calcium on fluid flux in lungs isolated from male Sprague Dawley rats perfused with saline (containing 4% albumin) or with whole blood. Lungs were allowed to equilibrate for a period of 30 min without treatment (controls), or with one of the following agents: the exogenous NO donor spermine NONOate, the nitric oxide synthase inhibitor N_-nitro-L-arginine (L-NNA;), 8-bromo cGMP, the calcium ionophore ionomycin, or the endothelial injurious agent protamine. Following equilibration, perfusate reservoir height was increased to five incremental settings to increase pulmonary venous pressure and enhance fluid flux. Perfusate reservoir weight was monitored continuously as an index of fluid flux. Lung wet/dry weight was determined upon completion of the experiments. Increasing reservoir height was associated with an increase in pulmonary arterial, pulmonary capillary and pulmonary venous pressures, and an increase in fluid flux. However, treatment with exogenous NO or inhibition of endogenous NO was without effect on fluid flux in saline lungs at two different flow rates or in whole blood perfused lungs. Similarly, treatment with cGMP and ionomycin did not alter fluid flux. Protamine pretreatment resulted in a significant increase in fluid flux at the highest reservoir setting, although exogenous NO and L-NNA pretreatments were without further effect on the protamine treated lungs. Thus, a role for NO and the second messengers cGMP and Ca2+ in modulating fluid flux could not be demonstrated in the isolated rat lung.

Received 3 March 1995; accepted in final form 16 August 1995.
APS Manuscript Number A237-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 August 1995.