α-肾上腺素能受体在脓毒症致ARDS中的作用机制

Effect mechanism of α-adrenoceptor on sepsis-induced acute respiratory distress syndrome

急性呼吸窘迫综合征（ARDS）是由严重创伤、感染、休克等多种非心源性因素导致的急性低氧性呼吸功能不全或衰竭，是多器官功能衰竭（MOF）在肺部的表现；其最常见的病因是能够引起机体失控反应的脓毒症。严重感染状态作为一种强烈的应激源，可引发机体强烈的应激反应。应激反应时，下丘脑-垂体-肾上腺皮质（HPA）轴及交感-肾上腺髓质轴兴奋，通过产生促肾上腺皮质激素（ACTH）、糖皮质激素（GC）、肾上腺素及去甲肾上腺素（NE）参与应激反应的发生发展。作为应激反应主要物质基础的儿茶酚胺（肾上腺素和NE）与肾上腺素能受体（AR）结合后，可通过复杂的信号转导途径发挥作用。因此，探讨α-AR激活后的信号转导途径对于揭示脓毒症致ARDS具有重要意义。

Acute respiratory distress syndrome （ARDS）, characterized by acute hypoxic respiratory dysfunction or failure, is a manifestation of multiple organ failure （MOF） in the lung, which often caused by various non-cardiac reasons, included severe trauma, infection, shock; and the most common risk factor is sepsis which would cause uncontrolled host response to infecting factors. As a strong stressor during sepsis, the severe infectious state of the body triggers serious stress reaction. The hypothalamus-pituitary-adrenal cortical （HPA） axis and sympathetic-adrenal medulla axis were activated and participated the initiation and progression of the stress response through the production of adrenocorticotropic hormone （ACTH）, glucocorticoid （GC）, epinephrine and norepinephrine （NE）. As the main hormones during sepsis, catecholamines （CA）, including epinephrine and NE, could bind to adrenergic receptor （AR）. After the binding, CA could play its role through the complicated signal way. Therefore, to explore the signal transduction pathway of α-AR, during sepsis, is important for revealing the mechanism of sepsis-induced ARDS.