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J Appl Physiol 87: 47-53, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 1, 47-53, July 1999

Inhaled NO preadministration modulates local and remote ischemia-reperfusion organ injury in a rat model

Benoit Guery1, Remy Neviere2, Nathalie Viget1, Claude Foucher3, Patrice Fialdes3, Francis Wattel2, and Gilles Beaucaire1

1 Service de Réanimation Médicale et Maladies Infectieuses, Centre Hospitalier de Tourcoing, 59208 Tourcoing; 2 Service de Réanimation Médicale, Centre Hospitalier Régional et Universitaire de Lille, University of Lille II, 59045 Lille; and 3 Laboratoire de Biophysique, Centre Hospitalier Régional et Universitaire de Lille, 59037 Lille, France

Inhaled nitric oxide (iNO) has been shown to have a protective effect in lung ischemia-reperfusion (I/R)-induced injuries. We studied the role of iNO (10 parts/million for 4 h) administered before I/R. In an isolated perfused lung preparation, iNO decreased the extravascular albumin accumulation from 2,059 ± 522 to 615 ± 105 µl and prevented the increase in lung wet-to-dry weight ratio. To study the mechanisms of this prevention, we evaluated the role of nitric oxide (NO) transport and lung exposure with matched experiments by using either lungs or blood of animals exposed to iNO and blood or lungs of naive animals. iNO-exposed blood with naive lungs did not limit the extravascular albumin accumulation (2,561 ± 397 µl), but iNO-exposed lungs showed a leak not significantly different from the group in which both lungs and blood were iNO exposed (855 ± 224 vs. 615 ± 105 µl). An improvement in heart I/R left ventricular developed pressure in the animals exposed to iNO showed that blood-transported NO was, however, sufficient to trigger remote organ endothelium and reduce the consequences of a delayed injury. In conclusion, preventive iNO reduces the consequences of lung I/R injuries by a mechanism based on tissue or endothelium triggering.

endothelium triggering; lung permeability; heart ischemia-reperfusion-induced injury


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