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机构地区:[1]山西省吕梁市人民医院泌尿外科,离石033000 [2]山西医科大学第一医院泌尿外科,太原030001
出 处:《中国中西医结合肾病杂志》2008年第3期213-216,共4页Chinese Journal of Integrated Traditional and Western Nephrology
基 金:山西省科委重点攻关项目(No031057)
摘 要:目的:采用鼠婴肾组织肾包膜下移植的方法治疗大鼠的肾性贫血,进一步研究氧自由基对肾性贫血大鼠红细胞膜脂质过氧化物和Na+-K+ATP酶的影响。方法:以Wistar雄性大鼠建立慢性肾衰竭动物模型为受体,将鼠婴肾组织块多点植入受体肾包膜下。治疗期间监测血红蛋白(Hb)、红细胞(RBC)和血清肌酐(Scr)、血清尿素氮(BUN),红细胞膜脂质过氧化物(MDA)、超氧化物歧化酶(SOD)、Na+-K+ATP酶的活性。结果:60d时肾组织移植治疗组Hb含量(106±12)g/L高于模型对照组(80±5)g/L,P<0.05;RBC数(6.05±0.60)×1012/L高于模型对照组(5.15±0.23)×1012/L,P<0.05;红细胞SOD含量(1557±54)U/gHb增加,与模型对照组(1051±36)U/gHb比较,P<0.05;红细胞膜Na+-K+ATP酶水平(178.5±14.5)μmolp/gHb增加与模型对照组(88.7±20.1)μmolp/gHb比较,P<0.05;红细胞MDA含量(1.87±0.25)nmol/ml低于模型对照组(3.73±0.36)nmol/ml,P<0.05。结论:同种肾组织移植后氧自由基对红细胞膜的损伤程度减轻,膜的流动性增加,膜对Na+离子转运及能量代谢得到适当调整,稳定了红细胞膜的结构和功能。Objective: To study effction of RBC - SOD to RBC - MDA and Na^+ - K^+ ATPase in renal anemia rats caused by chronic renal failure , kidney tissue mass implantation into the capsule of rat kidney to treat anemia caused by chronic renal failure (CRF). Methods:After the models of chronic renal failue (CRF) induced by adriamyucin were set up in Wistar rats,the kidney tissue mass ( 1 mm3) of newborn Wistar rats were located under the capsule of kidney of the models. During the process of treatment, Hb, RBC, BUN, Scr in blood were tested by automatic analyzer, RBC- SOD, RBC- MDA , Na^+ -K^+ ATPase level were tested. Results: the levels of I/b(106 ± 12) g/L, RBC(6.05 ± 0. 60) × 10^12/L in blood kept on increasing in the period of implantation and were higher than Hb(80 ± 5 ) g/L, RBC(5.15 ± 0.23) × 10^12/L, RBC - SOD( 1 557 ± 54) U/g Hb, RBC - MDA( 1.87 ± 0.25 ) nmol/ml, Na^ + -K^ + ATPase leve( 178.5 ± 14.5)μmolp/g Hb kept on increasing in the period of implantation and were higher than RBC - SOD( 1051 ± 36 ) U/g Hb, RBC - MDA(3.73 ± 0.36) nmol/ml, Na ^+ - K ^+ ATPase leve(88.7 ± 20.1 ) μmolp/g Hb in control group with the diffetence being significant( P 〈 0.05). Conclusion: Align-aft transplantation of kidney tissu mass can ameliorate renal anemia caused by chronic renal failure and might be anew therapeutic means to treat CRF induced anemia.
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