血管升压素是维持心血管功能稳定的重要内源性物质。但脓毒性休克时,其在体内却相对不足,给予外源性血管升压素可引起显著的血管升压效应。目前,脓毒性休克时机体血管升压素缺乏以及机体对其敏感性增高的具体机制尚不清楚。目前研究认为,血管升压素受体改变、收缩和舒张血管因素、自主神经系统和下丘脑-垂体-肾上腺轴均参与了血管升压素高敏感性机制的调节。 Vasopressin is an important endogenous substance that maintains the stability of cardiovascular function. However, septic shock, while it is relatively inadequate in vivo, given exogenous vasopressin can cause significant vasopressor effect. At present, the lack of body vasopressin in septic shock and the specific mechanism by which the body is sensitized are still unclear. The current study suggests that vasopressin receptor changes, vasoconstriction and relaxation, autonomic nervous system and hypothalamic-pituitary-adrenal axis are involved in the regulation of vasopressin hypersensitivity mechanism.