| The close relation between acute respiratory distress syndrome (ARDS) and multiple organ dysfunction syndrome (MODS) has been confirmed by clinical and experimental data. Most ARDS patients have one or more organ dysfunction besides lung injure. During the course of most MODS, ARDS always emerges before other organ dysfunction. ARDS is essentially an acute respiratory failure, which is characterized by progressing dyspnea and intractable hypoxemia. Intractable hypoxemia is not only the physiopathologic character of ARDS, but also one of the pathogenesies of subsequent multiple organ injure. Besides cell energy metabolism dysfunction and metabolic acidosis, the mechanisms of organ injured by hypoxia also involve the activation of inflammatory cells and releasing of many kinds of inflammatory factors. The aim of this study is to probe the following problems: (1) The effects of hypoxia on the concentrations of TNF-αand IL-1βin rat's plasma; (2) The main cell or tissue sources of the plasma TNF-αand IL-1βduring hypoxia; (3) The singnal pathway and regulatory mechanisms of TNF-αand IL-1βexpression in peripheral blood monocytes (PBMC) exposed to hypoxia.Methods: (1) The hypoxia model in rats was established by inhaling low-oxygen gas mixture (8 % O2, 5 % CO2, 87 % N2). The concentrations of TNF-αand IL-1βin plasma, lung, heart, liver and kidney were detected with enzyme linked immunoadsorbent assay (ELISA). The levels of TNF-αand IL-1βmRNA in peripheral blood mononuclear cells were detected with reverse transcription polymerase chain reaction (RT-PCR); (2) One hundred fourty-nine bottles of rat PBMC were randomly divided into three groups: hypoxia group, hypoxia+Chelerythrine group and hypoxia+Forskolin group. Each group was divided into seven subgroups: hypoxia 0, 1, 3, 6, 9, 12 and 24 h subgroups. The monocytes were subjected to hypoxia (3 % O2, 5 % CO2, 92 % N2) with or without 10μM Chelerythrine or 50μM Forskolin. The levels of TNF-αand IL-1βmRNA in monocytes...
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