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Background Pulmonary hypertension (PH) due to vasoconstriction and occlusion of the pulmonary microvasculature is a characteristic feature of the acute respiratory distress syndrome (ARDS). Inhaled nitric oxide (NO) selectively dilates the pulmonary vasculature by activating soluble guanylate cylase (sGC). Bay 41-2272 a novel sGC stimulator not only activates sGC NO independently, but also leads to synergistic effects when combined with NO. Because contradictory results of a number of experimental studies dealing with the effects of iNO in acute lung injury and the uncertain efficacy of iNO in the treatment of ARDS, we evaluated the effects of iNO and BAY 41-2272 in a model of acute lung injury. METHODS: Acute lung injury (ALI) was induced by i.v. injection of oleic acid (OA). In the first treatment group iNO (2 ppm) was administered continuously after ALI. In the second group, BAY 41-2272 (100 μg/kg) was infused for 10 min directly after injection of OA. In the third group, iNO and BAY 412272 were combined.

Inhaled NO and the guanylate cyclase stimulator Bay 41-2272 in oleic acid induced acute lung injury in rabbits