论文部分内容阅读
探讨急性肾功能衰竭 (以下简称为 ARF)时尿毒症毒素对肝的损害情况 ,为临床防治提供形态学依据。Wistar大白鼠 32只 ,随机分成正常对照组 ,14只 ;双输尿管结扎结扎组 ,18只。模型建成后 2 3- 37小时内将动物处死 ,取肝组织作NOS、 MAO、 SDH、 L DH、 Ch E、 ATPase、 ACP等项酶组织化学显色及超微结构观察。结果显示 :实验组 SDH、 Mg2 + -ATPase 的活性均由正常的强阳性 ( )下降为阳性 (+) ;MAO、 Ch E的活性均由正常的中等阳性 ( )下降为阳性(+) ;ACP、 L DH的活性均由阳性 (+)增强到中等阳性 ( ) ;NOS活性由正常的弱阳性 (± )增强为阳性 (+) ;肝细胞器结构受损。结果表明 :ARF的尿毒素的大量淤积通过影响肝脏酶的活性来干扰和抑制糖代谢、三羧酸循环、蛋白质合成及解毒等功能 ,并导致肝损害发生。 2用改良的 NADPH-黄递酶法可显示肝组织 NOS的存在 ,该法操作简便 ,经济 ,特别适用于同时需要留取活组织做其它检查者。当输尿管结扎时 ,NOS的确切作用有待于进一步探讨
To investigate the damage of liver caused by uremic toxins in patients with acute renal failure (ARF) for the purpose of providing morphological evidence for clinical prevention and treatment. Thirty-two Wistar rats were randomly divided into normal control group (n = 14), bilateral ureteral ligation group (n = 18). Animals were sacrificed within 2-3 hours after the model was established. Liver tissues were taken for histochemical staining and ultrastructure observation of NOS, MAO, SDH, L DH, ChE, ATPase and ACP. The results showed that the activities of SDH and Mg2 + -ATPase in the experimental group decreased from normal strong positive to positive, respectively. The activities of MAO and Ch E decreased from normal to positive, , L DH activity increased from positive (+) to moderately positive (); NOS activity increased from normal weak positive (+) to positive (+); and hepatic organelle structure was impaired. The results showed that the massive deposition of uremic toxin in ARF could interfere with and inhibit the function of glucose metabolism, tricarboxylic acid cycle, protein synthesis and detoxification by affecting the activity of hepatic enzymes, leading to liver damage. 2 with improved NADPH-diaphorase enzymatic method can show the existence of liver tissue NOS, the method is simple and economical, especially for biopsy also need to take other tests. When ureteral ligation, the exact role of NOS needs further study