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Department of Medicine, Division of Pulmonary and Critical Care Medicine, The Johns Hopkins Medical Institutions at the Asthma and Allergy Center, Hopkins Bayview Medical Center, Baltimore, Maryland 21224
We previously found that
increased intravascular pressure decreased ischemic lung injury by a
nitric oxide (NO)-dependent mechanism (Becker PM, Buchanan W, and
Sylvester JT. J Appl Physiol 84: 803-808, 1998).
To determine the role of cyclic nucleotides in this response, we
measured the reflection coefficient for albumin (
alb),
fluid flux (
), cGMP, and cAMP in ferret lungs
subjected to either 45 min ("short"; n = 7) or 180 min ("long") of ventilated ischemia. Long ischemic lungs had
"low" (1-2 mmHg, n = 8) or "high" (7-8 mmHg, n = 6) vascular pressure. Other long
low lungs were treated with the NO donor
(Z)-1-[N-(3-ammoniopropyl)-N-(n-propyl)amino]diazen-1-ium-1,2-diolate (PAPA-NONOate; 5 × 10
4 M, n = 6) or
8-bromo-cGMP (5 × 104 M, n = 6).
Compared with short ischemia, long low ischemia decreased alb (0.23 ± 0.04 vs. 0.73 ± 0.08;
P < 0.05) and increased (1.93 ± 0.26 vs. 0.58 ± 0.22 ml · min1 · 100 g1;
P < 0.05). High pressure prevented these changes. Lung
cGMP decreased by 66% in long compared with short ischemia. Lung cAMP did not change. PAPA-NONOate and 8-bromo-cGMP increased lung cGMP, but
only 8-bromo-cGMP decreased permeability. These results suggest that
ischemic vascular injury was, in part, mediated by a decrease in cGMP.
Increased vascular pressure prevented injury by a cGMP-independent mechanism that could not be mimicked by administration of exogenous NO.
cGMP; cAMP; lung injury; reflection coefficient; filtration coefficient
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