麻醉科医生在外科术后康复中的作用麻醉版模板.ppt

* Iron haemostasis and inflammation. Inflammation, whether caused by infection, malignant cells or auto-immune mechanisms, involves the activation of T cells and monocytes, triggering a cascade of responses. This inflammatory cascade alters the haemostasis of iron and limits its availability for erythropoiesis. Inflammation and increased iron levels up-regulate hepcidin, which inhibits duodenal absorption of iron. Individual macrophages are stimulated by inflammatory mediators to take up Ferrous iron (Fe2+). Inflammatory mediators also up-regulate the expression of transferrin receptors, increasing the uptake of transferrin bound iron into the macrophage. Transferrin, the protein that binds and transports iron, can be functionally blocked from carrying out its role due to increased levels of hepcidin. Activated macrophages phagocytose ageing red blood cells at the end of their lifespan (approximately 120 days) permitting the recycling of iron. The transmembrane iron transporter ferroportin is down-regulated by hepcidin, reducing iron transport out of the macrophage and duodenal enterocyte. Thus, a state of functional iron deficiency is created as a consequence of the sequestration of iron within the duodenum and macrophages in response to the effects of inflammatory mediators. Tumour necrosis factor alpha (TNF-a) can induce macrophages and damage red blood cells membranes, leading to early phagocytosis. Inflammatory mediators additionally reduce erythropoietin production by the kidney, reducing erythropoiesis [32]. (Adapted with permission from: Richards, T. Anaemia in hospital practice. British Journal of Hospital Medicine 2012; 73: 571–5 ①铁平衡的关键因素是铁调素（Hepdin）；②炎症刺激T淋巴细胞和单核细胞，启动炎症瀑布；③炎症介质上调Hepdin，而铁调素抑制十二指肠吸收铁； ④巨噬细胞在炎症介质的刺激下摄取二价铁增多； ⑤炎症介质上调转铁蛋白受体，加速巨噬细胞摄取转铁蛋白结合的铁；⑥铁调素阻断转铁蛋白的功能；⑦铁调素下调膜铁转运蛋白，从而阻止肠道吸收铁；⑧炎症反应还抑制肾脏生成促红细胞生成素（EPO） ③ * Peripheral afferent neuronal barrage from tissue injury produces central nervous system hyperexcitability which may contribute to increase