ABSTRACTThis study examines the hypothesis that neutrophils isolated from animals sustaining intestinal reperfusion (IIR) induce pulmonary microvascular dysfunction. Lungs were isolated from normal Sprague-Dawley rats and perfused with a physiologic bufferin vitro. Neutrophils (2 times; 106) isolated from animals sustaining IIR (n equals; 5) or sham operation (SHAM; n equals; 6) were infused into the isolated lung model. A third group of lungs underwentin vitroperfusion without exposure to neutrophils (n equals; 5). Lung injury was assessed by measuring wet to dry weight ratios and pulmonary artery pressure (PAP). Pulmonary ultrastructure was assessed by electron microscopy. The wetcolon;dry ratio of lungs from animals sustaining IIR was greater than that of lungs exposed to SHAM neutrophils (pequals; .03) or perfusate alone (pequals; .02). The PAP of lungs exposed to IIR neutrophils was nearly 10 times greater than that of lungs exposed to SHAM neutrophils (pequals; .003) or buffer alone (pequals; .006). Ultrastructural examination of lungs exposed to IIR neutrophils demonstrated interstitial edema with occasional focal disruptions in the alveolar capillary endothelial cell membrane whereas lungs exposed to SHAM neutrophils were normal. These experiments provide importantin vitrocorrelation of priorin vivostudies suggesting that neutrophils are important pathogenic mediators of IIR-induced lung injury.
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