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尽管对重危外科监护和抗微生物治疗有了很大的进展,但合并革兰氏阴性菌败血症的成人呼吸窘迫综合征(ARDS)死亡率仍高于80%。ARDS实际上是反映多个器官受累的宿主防御机能失调的一部分。用细菌内毒素(脂多糖类,即LPS)激活的巨噬细胞能引起多种生物学的强烈细胞分裂,后者可传递炎症和败血症的病理生理学反应。这种炎性网状结构的核心是肿瘤坏死因子(TNF-α),为内毒素性休克的主要内源性介体。近来认为,TNF是引起ARDS的病因。Millar等已证明,在ARDS病人的支气管肺分泌物中TNF-α值升高。为了进一步叙述ARDS并有肝功能衰竭与肝肺巨噬细胞轴所致的特异性变化的关系,作者对TNF-α和由LPS刺激Kupffer细胞(KC(?))和肺泡巨噬细胞(AMs)的产物白细胞介素-6(IL-6)的动力学进行了比较。结果用5×10~5个KC经2.5 mg/L细菌的LPS
Despite great advances in critical care and antimicrobial therapy, mortality from adult respiratory distress syndrome (ARDS) combined with Gram-negative septicemia remains above 80%. ARDS is actually part of a host defense disorder that reflects multiple organ involvement. Macrophages activated with bacterial endotoxins (lipopolysaccharides, ie, LPS) cause a multitude of biological intense cell divisions that transmit the pathophysiological responses to inflammation and sepsis. The core of this inflammatory reticular formation is tumor necrosis factor (TNF-α), the major endogenous mediator of endotoxic shock. Recently, it is thought that TNF is the cause of ARDS. Millar et al. Have demonstrated elevated TNF-alpha levels in bronchial lung secretions of ARDS patients. To further elucidate ARDS and the relationship between hepatic failure and specific changes in the liver-lung macrophage axis, we investigated the effects of TNF-α and Kupffer cells stimulated by LPS (KC (?)) And alveolar macrophages (AMs) The product of interleukin-6 (IL-6) kinetics were compared. Results LPS with 2.5 mg / L bacteria was used at 5 × 10 ~ 5 KC