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Effect of time and vascular pressure on permeability and cyclic nucleotides in ischemic lungs
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 n...
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Published in: | American journal of physiology. Heart and circulatory physiology 2000-11, Vol.279 (5), p.H2077-H2084 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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 × 10 4 M, n = 6).
Compared with short ischemia, long low ischemia decreased alb (0.23 ± 0.04 vs. 0.73 ± 0.08;
P |
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ISSN: | 0363-6135 1522-1539 |
DOI: | 10.1152/ajpheart.2000.279.5.h2077 |