Exhaled nitric oxide and acute lung injury in a rat model of extracorporeal circulation.

Exhaled nitric oxide (NO) concentration, a marker of pulmonary inflammation, has been shown to be elevated in various models of acute lung injury (ALI). This study was undertaken to evaluate the pulmonary NO production in a rat model of postextracorporeal circulation (ECC) ALI. Wistar rats underwent either a partial femorofemoral ECC in normothermia for 3 h (n = 10) or a sham procedure (n = 10). The extracorporeal circuit consisted of a roller pump and a membrane oxygenator. Exhaled NO concentration was monitored with a chemiluminescence analyzer. After sacrifice, lungs were harvested for microscopic studies and to analyze the inducible nitric oxide synthase (iNOS) activity and expression (Western blot). ECC was responsible for an ALI characterized by a decreased arterial blood oxygen saturation (88.9% [51.7-94.2] vs. 93.7% [91.4-98.6] P = 0.005) and pulmonary histological changes (marked alveolar neutrophil infiltration; interstitial edema; intraalveolar hemorrhage). The lung injury score was significantly higher in the ECC group (n = 5; 3.0 [2-4]) in comparison to the sham group (n = 5; 1.0 [0-2]). Exhaled NO concentration remained stable throughout the experiment in all sham rats whereas it significantly increased in the ECC group from baseline (2 ppb [1-5]) until the end of experiment (33.5 ppb [1-47]). Lung iNOS activity and expression were also significantly increased in the ECC group. An increase in exhaled NO, however, did not correlate with the decrease in arterial oxygen pressure. ECC was responsible for an ALI in rats and for an elevated pulmonary NO production. Determination of the relationship between exhaled NO and the severity of the inflammatory process in ALI will require further studies.