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Attenuation of Reperfusion-Induced Systemic Inflammation by Preconditioning With Nitric Oxide in an In Situ Porcine Model of Normothermic Lung Ischemia^*

^* From the Cardiovascular Institute (Drs. Waldow, Alexiou, Witt, Gulielmos, Matschke, and Knaut), University Hospital Dresden, Dresden; and the Department of Cardiovascular Surgery (Dr. Wagner), University Hospital Eppendorf, Hamburg, Germany.

Correspondence to: Thomas Waldow, MD, Herzzentrum Dresden, Klinik für Kardiochirurgie, Fetscherstr. 76, 01307 Dresden, Germany

Study objectives: Inhalation of nitric oxide (NO) can ameliorate pulmonary ischemia/reperfusion (I/R) injury of the lung in several experimental models, but toxic effects of NO were also reported. Here we investigate whether NO inhalation for a short period prior to surgery is sufficient to prevent symptoms of lung I/R injury, especially the inflammatory response.

Design: Using an in situ porcine lung model, normothermic left lung ischemia was maintained for 90 min, followed by a 5-h reperfusion period (group 1, n = 7). In group 2 (n = 6), I/R was preceded by inhalation of NO (10 min, 15 ppm). Animals in group 3 (n = 7) underwent sham surgery without NO inhalation or ischemia.

Measurements: Oxygenation and hemodynamic parameters were measured as indicators of lung functional impairment. Plasma levels of interleukin (IL)-1ß, IL-6, and transforming growth factor (TGF)-ß1 were determined throughout the I/R maneuver. In addition, tissue macrophages were analyzed by lectin binding.

Results: Symptoms of I/R injury (pulmonary hypertension and decreased oxygenation) in group 1 animals were attenuated by NO inhalation. The reperfusion-induced increases of the levels of IL-1ß and IL-6 in plasma were reduced by NO pretreatment. A peak of TGF-ß1 immediately after NO administration was observed in group 2, but not in groups 1 and 3. There was no significant effect of NO on tissue macrophages.

Conclusion: NO inhalation for a short period prior to lung I/R is sufficient to protect against pulmonary hypertension, impaired oxygenation, and the inflammatory response of pulmonary I/R injury.

Key Words: cytokine • inflammation • lung • nitric oxide • pig • preconditioning • reperfusion injury

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