肝硬化对大鼠离体十二指肠电性自律性的影响

Gholamreza Bayat, A. Khalili, Marjan Hosseini, Roham Mazloom
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引用次数: 0

摘要

背景:肝硬化减少了小肠蠕动和转运时间,机制尚不清楚。此外,肠道运动依赖于Cajal (ICC)间质细胞的电活动和自律性。如果肝硬化直接影响肠道运动的内在机制,那么肝硬化患者的离体肠也会出现与正常患者相比的电异常。目的:探讨肝硬化对大鼠离体十二指肠电性自律性的影响。材料与方法:胆管结扎(BDL)术后6周麻醉动物,取心脏采血,评价血浆肝硬化指标,包括体重、血浆白蛋白、血清谷草酰乙酸转氨酶(SGOT)、血清谷丙转氨酶(SGPT)、胆红素、直接胆红素。然后分离大鼠十二指肠,与对照组比较电慢波频率和最大慢波振幅。结果:对照组与BDL组在体重、血浆白蛋白、SGOT、SGPT、胆红素和直接胆红素方面均有显著差异。此外,与对照组相比,BDL组的最大慢波幅度显著降低。结论:似乎不同的因素直接损害了ICC网络,如肝硬化引起的微生物群扩增引起的炎症,从而降低了小肠的运动性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Effects of Liver Cirrhosis on Electrical Autorhythmicity of Isolated Duodenum in Rats
Background: Cirrhosis reduced small bowel motility and transit time, with unknown mechanisms. Moreover, intestinal motility depends on the electrical activity and the autorhythmicity of interstitial cells of Cajal (ICC). If cirrhosis directly affects the intrinsic mechanism of intestinal motility, the isolated bowel of cirrhotic cases will also exhibit an electrical abnormality compared with normal cases. Objectives: This study aimed to identify the effects of liver cirrhosis on the electrical autorhythmicity of isolated duodenum in rats. Materials and Methods: Six weeks after bile duct ligation (BDL) surgery, animals were anesthetized, and blood samples were obtained from the heart for the evaluation of plasma cirrhosis indices, including weight, plasma albumin, serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), bilirubin, and direct bilirubin. Then, the duodenum of rats was isolated and compared with the control group for the rate of electrical slow waves and the maximum amplitude of slow waves. Results: Significant differences were observed between the control and BDL group in terms of weight, plasma albumin, SGOT, SGPT, bilirubin, and direct bilirubin. Moreover, there was a significant decrease in the maximum amplitude of slow waves in the BDL group compared with the control. Conclusion: It seems that different factors directly harm the ICC network such as inflammation caused by microbiome amplification as a result of cirrhosis, which in turn reduces small bowel motility.
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