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In this study we investigated the role of lymphatic system on the mechanisms associated to the induction of lung inflammation afier intestinal IIR in rats. The hypothesis ofthe study was that upon intestinal IIR, inflarnmatory mediators are generated in the intestine and once drained by mesenteric lyrnphatic system interfere with the lung homeostasis contributing to lung dysfunction observed in ARDS. To these purposes groups of rats were submitted to occlusion of superior mesenteric artery (45 min) followed by intestinal reperfusion during 2h when the rats were killed. Groups of rats were subjected to thoracic lymphatic duct ligation previously to induction of the intestinal I/R. The data showed that the thoracic duct ligation significantly reduced the increased pulmonary MPO activity and the augrnented vascular perrneability (extravasation of the Evans blue dye) in lung and intestine. In addition, thoracic duct ligation increased the intestinal activity of LDH. Systemically, the obstruction of lymph flow, leaded to reduction of TNF in serum of rats upon intestinal I/R and increased the levels of IL-IO, LTB4 and TXB2. Elevated levels ofTNF-o., IL-ll), IL-IO, LTB4 and TXB2 were also found in lymph ofrats upon intestinal I/R. The treatment of the animals previously to the intestinal I/R induction with inhibitor of TNF-o. synthesis, pentoxyfilline (PTX), reduced the lung MPO activity upon lymphatic duct intact that was exacerbated by thoracic duct ligation. PfX treatment reduced the increased vascular perrneability of the lung and intestine conditions in rats with lymphatic duct intact. On the other hand, when the thoracic duct was ligated, the PfX did not cause additional reduction of vascular perrneability in both tis sues , but reduced the serum levels of IL-I I) and increased those of LTB4. Lymph of rats treated with PfX revealed an increased leveI of IL-I O and LTB4 and a reduced leveI of IL-l I) and TXB2. L-NAME treatment increased the serum levels of TNF-o., which were reduced by the thoracic lymphatic duct ligation. The blockade of NO synthesis in rats with lymphatic duct ligation did not modify the IL-10 serum levels, but increased those of IL-I 1).Lymph of rats upon LNAME treatment, an increased levei of IL-Il), IL-lO, LTB4 and TXB2 and a reduction of TNF-o. levels were detected. Pulmonary tissue of Iymphatic duct intact rats afier intestinal I/R were increased the release of IL-I I) and IL-IO whereas the thoracic duct ligation reduced the release of these cytokines. PTX treatment reduced the levels of IL-I I) and increased the IL-IO in the lung. LNAME treatment increased the IL-II) and IL-IO in lung ofintact duct rats but the obstruction of lymph flow caused an increase release of IL-I f3levels. Intestinal I/R in intact duct rats, increased whereas the thoracic duct ligation reduced the pulmonary expression ofICAM-I, Mac-I and Eselectin. In conclusion, our data suggest that intestinal I/R, induces the generation of local inflammatory mediators (intestine) which drained by the mesenteric lymphatic system are carried by the lymph and reach the lung. ln these conditions we observed pulmonary inflammation and additional generation of inflammatory mediators and eventually the development of the systemic inflammation. Our data support the view that lymphatic system play a role a path underlying the spread oflung and gut injury after intestinal IIR.

Avaliação do envolvimento do sistema linfático na inflamação pulmonar decorrente de trauma esplâncnico.