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Vol. 84, Issue 3, 803-808, March 1998
Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
Cessation of blood
flow during ischemia will decrease both distending and shear
forces exerted on endothelium and may worsen ischemic lung injury by
decreasing production of nitric oxide (NO), which influences vascular
barrier function. We hypothesized that increased intravascular pressure
(Piv) during ventilated ischemia might maintain NO production
by increasing endothelial stretch or shear forces, thereby attenuating
ischemic lung injury. Injury was assessed by measuring the filtration
coefficient
(Kf) and the
osmotic reflection coefficient for albumin
(
alb) after 3 h of ventilated
(95% O2-5%
CO2; expiratory pressure 3 mmHg) ischemia. Lungs were flushed with physiological salt solution, and then Piv was adjusted to achieve High Piv (mean 6.7 ± 0.4 mmHg, n = 15) or Low Piv (mean
0.83 ± 0.4 mmHg, n = 10).
NG-nitro-L-arginine methyl ester
(L-NAME;
10
5 M,
n = 10),
NG-nitro-D-arginine
methyl ester (D-NAME;
105 M,
n = 11), or
L-NAME
(105
M)+L-arginine (5 × 104 M,
n = 6) was added at the start of
ischemia in three additional groups of lungs with High Piv.
High Piv attenuated ischemic injury compared with Low Piv
(alb 0.67 ± 0.04 vs. 0.35 ± 0.04, P < 0.05). The
protective effect of High Piv was abolished by
L-NAME
(alb 0.37 ± 0.04, P < 0.05) but not by
D-NAME
(alb 0.63 ± 0.07). The effects of L-NAME were overcome
by an excess of L-arginine
(alb 0.56 ± 0.05, P < 0.05).
Kf did not differ
significantly among groups. These results suggest that Piv modulates
ischemia-induced barrier dysfunction in the lung, and these
effects may be mediated by NO.
osmotic reflection coefficient; vascular permeability; acute lung injury
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