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Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins Medical Institutions at the Asthma and Allergy Center, Hopkins Bayview Medical Center, Baltimore, Maryland 21224
Ventilation during ischemia attenuates
ischemia-reperfusion lung injury, but the mechanism is unknown.
Increasing tissue cyclic nucleotide levels has been shown to attenuate
lung ischemia-reperfusion injury. We hypothesized that
ventilation prevented increased pulmonary vascular permeability during
ischemia by increasing lung cyclic nucleotide concentrations.
To test this hypothesis, we measured vascular permeability and cGMP and
cAMP concentrations in ischemic (75 min) sheep lungs that were
ventilated (12 ml/kg tidal volume) or statically inflated with the same
positive end-expiratory pressure (5 Torr). The reflection coefficient
for albumin (
alb) was 0.54 ± 0.07 and 0.74 ± 0.02 (SE) in nonventilated and ventilated
lungs, respectively (n = 5, P < 0.05). Filtration coefficients
and capillary blood gas tensions were not different. The effect of
ventilation was not mediated by cyclic compression of alveolar
capillaries, because negative-pressure ventilation
(n = 4) also was protective (alb = 0.78 ± 0.09). The
final cGMP concentration was less in nonventilated than in ventilated
lungs (0.02 ± 0.02 and 0.49 ± 0.18 nmol/g blood-free dry wt,
respectively, n = 5, P < 0.05). cAMP concentrations were
not different between groups or over time. Sodium nitroprusside
increased cGMP (1.97 ± 0.35 nmol/g blood-free dry wt) and
alb (0.81 ± 0.09) in
nonventilated lungs (n = 5, P < 0.05). Isoproterenol increased
cAMP in nonventilated lungs (n = 4, P < 0.05) but had no effect on
alb. The nitric oxide synthase
inhibitor NG-nitro-L-arginine methyl
ester had no effect on lung cGMP (n = 9) or alb
(n = 16) in ventilated lungs but did
increase pulmonary vascular resistance threefold
(P < 0.05) in perfused sheep lungs (n = 3). These results suggest that
ventilation during ischemia prevented an increase in pulmonary
vascular protein permeability, possibly through maintenance of lung
cGMP by a nitric oxide-independent mechanism.
guanosine 3',5'-cyclic monophosphate; adenosine 3',5'-cyclic monophosphate; lung injury; reflection coefficient; filtration coefficient
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