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肾脏是体内合成前列腺素E_2(PGE_2)的重要器官。PGE_2可促进肾脏钠水排泄,扩张肾内小血管,参与调节机体水电解质平衡,维持肾脏血流动力学稳定。本研究拟探讨肾移植术后移植肾合成分泌PGE_2的变化及与尿电解质排泄的关系。用放射免疫法对照观察了15例肾移植术后半年以上的肾功能稳定者和21例发生急性排斥的肾移植者,以正常人为对照组。结果发现移植肾功能稳定者尿PGE_2、钠及钾离子含量和正常人无显著差异,尿中PGE_2浓度和尿钠浓度成正比;发生移植肾急性排斥时,尿钠排泌量减少,尿PGE_2浓度明显升高,与尿钠浓度相关性消失。两组肾移植者尿PGE_2与尿钾排泄均无明显卡相关。分析认为移植肾PGE_2分泌改变及其与尿钠排泌相关性的受损,是引起急性排斥时患者水钠潴留及移植肾血流动力学紊乱的原因之一。
Kidneys are important organs for the synthesis of prostaglandin E_2 (PGE_2) in the body. PGE 2 can promote the excretion of sodium and water in the kidneys, dilate the small blood vessels in the kidney, participate in the regulation of water and electrolyte balance in the body and maintain the hemodynamics of the kidney. This study was to investigate the changes of PGE_2 secretion and its relationship with urinary electrolyte excretion after renal transplantation. Radioimmunoassay control observed in 15 cases of kidney function more than six months after renal transplantation stable and 21 cases of acute rejection of renal transplant recipients to normal control group. The results showed that urine PGE 2, sodium and potassium levels in stable renal transplant recipients were not significantly different from those in normal subjects. PGE 2 concentration in urine was positively correlated with urinary sodium concentration. Urine sodium excretion was decreased and urinary PGE 2 concentration Significantly increased, and urine sodium concentration disappeared. There was no significant correlation between urinary PGE 2 and urinary potassium excretion in both groups. Analysis suggests that changes in the secretion of PGE 2 in renal transplant recipients and their association with impaired urinary sodium excretion is one of the causes of water-sodium retention and graft-versus-hemodynamic disturbances in patients with acute rejection.