临床面临的心肾联合损害问题

心肾同为循环系统上的两个重要器官,不仅通过血管相互连接,还通过内分泌效应[心脏:A型利钠肽、B型利钠肽;血管:内皮素、一氧化氮;肾脏:肾素、血管紧张素-2、醛固酮,促红细胞生成素(EPO)]和交感肾上腺系统(盐皮质激素、儿茶酚胺)保持着密切的联系.生理状态下,两器官借助血流动力学、神经内分泌、血管生物学途径,通过对血流动力、血管容量、血液容量的调控,发挥着稳定循环系统的作用.两个器官相互依存、相互调节、相互补充,维持内环境稳定.

Objective:The present study was designed to test the hypothesis that inflammation is involved in the end-organ damage(EOD) induced by sinoaortic denervation(SAD) in rats.Method:SAD was performed in male Sprague-Dawley rats at the age of 10 weeks.Under anaesthesia,aortic nerves were cut and the sinus region of the carotid artery was stripped and painted with 10% phenol.Pathological evaluation of EOD and the determination of plasma or tissue levels of the factors related to inflammation,including thromboxane B2(TXB2) interleukin-1(IL-1),tumour necrosis factor α(TNF-α) and reactive oxygen species(ROS) were performed at 16 weeks after SAD.Pathological evaluation of EOD included heart weigh ratio,myocardial and blood vessel hydroxyproline and collagen volume fraction,glomerular injury score and number of infiltrating inflammatory cells.Indomethacin(20 mg/kg per day,orally) or vitamin E(100 mg/kg per day,orally) was administered for 12 weeks,beginning from4 weeks after SAD,to observe their effects on SAD-induced EOD.Results:There were significant fibrosis and inflammatory infiltration in the myocardium and blood vessels,represented by higher hydroxyproline and collagen volume fraction,and a large amount of inflammatory cells in the tissues of SAD rats.Heart weight and kidney glomerular injury score were significantly higher in ed significantly after SAD.Indomethacin and vitamin E significantly decreased the contents of some factors related to inflammation in SAD rats.Both drugs also alleviated myocardial and vessel fibrosis,inflammatory infiltration and kidney damage.Conclusion:Inflammation is involved in the organ damage induced by SAD in rats.