Gut ischemia/reperfusion activates lung macrophages for tumor necrosis factor and hydrogen peroxide production

BACKGROUND: Gut ischemia followed by reperfusion (I/R) is implicated as a prime initiating event in the mechanism of multiple organ failure after trauma and hemorrhagic shock. Several lines of evidence indicate that macrophages are involved in this prime event. Our purpose was to evaluate hydrogen peroxide (H2O2) and tumor necrosis factor (TNF) production and phagocytosis by lung macrophages in a gut I/R model of multiple organ failure in rats. METHODS: In the experimental group (I/R), Wistar rats (n = 35) were anesthetized and subjected to a median laparotomy, and the superior mesenteric artery was clamped for 45 minutes followed by 60 minutes of reperfusion. In the control group (LAP) (n = 37), animals underwent sham laparotomy. After the period of reperfusion, bronchoalveolar lavage (BAL) was performed and the resulting BAL cells were assayed for H2O2 production using the horseradish peroxidase-mediated red phenol oxidation method. TNF release was determined using the L929 cells bioassay. Zymosan phagocytosis by BAL macrophages was quantitated using phase microscopy. RESULTS: H2O2 release in BAL cells of I/R rats (19.90 +/- 7.98 nmol/L/2 x 10(5) cells) is statistically higher than in the LAP group (10.92 +/- 5.01 nmol/L per 2 x 10(5) cells) (p = 0.0155), and the TNF production by BAL cells of the I/R group (38.09 +/- 20.79 units per 10(6) cells) was significantly higher than that of LAP rats (17.16 +/- 13.35 units per 10(6) cells) (p = 0.0281). Phagocytic activity of BAL mac. Macrophages of I/R rats was not statistically different from LAP animals. CONCLUSION: These results suggest that BAL macrophage play a role in the mechanism of acute lung injury after trauma and hemorrhagic shock.