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作 者:刘志强[1] 吕浩[2] 杨立群[2] 孙玉明[2] 李泉[2] 俞卫锋[2]
机构地区:[1]同济大学附属第一妇婴保健院麻醉科,上海200040 [2]第二军医大学东方肝胆外科医院麻醉科,上海200438
出 处:《第二军医大学学报》2008年第7期796-799,共4页Academic Journal of Second Military Medical University
基 金:国家自然科学基金(30600584)~~
摘 要:目的:探讨胆管阻塞对大鼠肝脏功能和病理形态学的影响。方法:60只健康雄性SD大鼠随机分为6组:胆总管结扎组(BDL,n=50)和假手术组(n=10,仅游离胆总管不予结扎)。BDL组据结扎持续时间又分为BDL3、BDL7、BDL14、BDL28和BDL42组(每组10只),分别于术后第3、7、14、28、42日测定血清总胆红素(TBIL)、直接胆红素(DBIL)、总胆汁酸(TBA)、谷丙转氨酶(ALT)等肝功能指标,并观察肝脏组织病理形态。假手术组于术后7d行上述检测。结果:与假手术组相比,BDL组大鼠肝脏功能指标明显改变,血清TBIL、DBIL、TBA值在阻塞早期(BDL3或BDL7组)为最高,后呈下降趋势,至实验末期(BDL42组)时仍高于对照组;ALT等酶学指标也有类似变化。BDL组大鼠的主要病理形态学改变为肝内小胆管增生和肝纤维化。结论:大鼠肝脏功能阻塞早期即发生明显的损害,机体可产生一定的代偿以改善肝功能,但持续存在的胆管阻塞最终导致肝纤维化。大鼠阻塞性黄疸期内病理形态学的改变显示其肝功能测定值并不能反映其肝脏组织的实际损害程度。Objective:To study the effect of obstructive jaundice on liver function and pathomorphology in rats. Methods: Sixty healthy male Sprague Dawley rats were randomly divided into bile duct ligation (BDL) group (the common bile ducts were ligated,n=50) and sham group(the common bile ducts were isolated but not ligated,n= 10). According to the ligation periods, BDL group was further divided into BDL3 , BDL7 , BDL14 , BDL28 and BDL42 groups. Liver function indices, including the serum total bilirubin(TBIL),direct bilirubin(DBIL),total bile acid(TBA), and alanine aminotransferase(ALT), were measured; and the liver pathomorphology was observed 3,7,14,28, and 42 days after BDL. The above examinations were performed in the sham rats 7 days after operation. Results. The liver function of rats had obvious changes compared with that of sham group. The serum levels of TBIL,DBIL,and TEA reached the peak in the early phases (BDL3 or BDL7 ) and decreased gradually thereafter, but were still higher than that of the sham control in the end phase(BDL42 ). There was a similar change in the biochemical indices such as ALT. The main pathomorphology changes in BDL group were intrahepatic bile duct proliferation and hepatic fibrosis. Conclusion: There is obvious impairment in the early phase of obstructive jaundices the liver function may be improved to a certain degree by a compensation mechanism; however, the persistence of obstructive jaundice finally leads to hepatic fibrosis. The liver function indicated by the pathomorphology changes can not reflect the actual impairment of liver tissue in obstructive jaundice rats.
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