Inhaled NO attenuates I/R-induced pulmonary microvascular leak, which requires sGC activation and may involve a mechanism independent of inhibition of leukocyte-endothelial cell interactions. In addition, INO is ineffective in reversing I/R-induced microvascular leak.

Intravenous administration of diaspirin crosslinked hemoglobin (DCLHb) can result in elevated pulmonary and systemic arterial pressures in some mammalian species. This study was designed to evaluate the ability of inhaled nitric oxide (INO) to attenuate elevations in pulmonary artery pressure in a closed-chested swine model. Yorkshire pigs received escalating doses of INO followed by escalating doses of DCLHb or a single dose of DCLHb followed by escalating doses of INO. Systemic and pulmonary arterial pressures were monitored continuously. Significant elevations occurred in systemic and pulmonary arterial pressure following a cumulative dose of 0.1 gm/kg DCLHb. A single dose of 0.3 gm/kg also resulted in elevations of pulmonary and systemic arterial pressure. Inhaled nitric oxide partially reversed the changes in pulmonary but not systemic pressure. These results indicate that INO might be a therapeutic option for humans who may experience increased pulmonary artery pressure following administration of DCLHb.

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