交感神经激活在自体动静脉内瘘新生内膜增生中的作用

The role of sympathetic nerve activation in neointimal hyperplasia of autogenous arteriovenous fistula

自体动静脉内瘘(arteriovenous fistula,AVF)是血液透析治疗最常用的血管通路。然而,AVF失功问题严重制约着其临床应用,静脉流出道狭窄是AVF失功的常见原因,其病理基础是新生内膜增生(neointimal hyperplasia,NIH)。NIH的发生发展与血管内病理机制有关,包括炎症、氧化应激等一系列级联反应和血管重塑,导致血管狭窄、失功。终末期肾病患者存在交感神经的过度激活,而交感神经的激活可能通过不同的机制参与NIH的发生而导致AVF的失功。本综述重点阐述交感神经激活参与NIH发生发展的可能机制,旨在为AVF失功提供新的理论解释及其防治提供新的干预靶点。

Autologous arteriovenous fistula(AVF)is the most important route of blood access for hemodialysis,and failure of AVF may seriously limit its clinical application.Stenosis in venous outflow tract is a common cause of AVF failure,pathologically due to the neointimal hyperplasia(NIH).The mechanisms underlying NIH include a series of cascade reactions in local vessels,such as inflammation,oxidative stress and vascular remodeling,leading to vascular stenosis and AVF failure.On the other hand,hyperactive sympathetic nerve function is frequently present in end stage renal disease patients,which may also take part in the occurrence of NIH and AVF dysfunction through several pathways.This review focuses on the possible mechanisms of sympathetic activation to the development of NIH,aiming to provide a new theoretical explanation and a new intervention target for the prevention and treatment of AVF failure.