肝源性糖尿病发病机理及其治疗体会

本文阐述了肝源性糖尿病发病机理、临床表现、治疗要点及其治疗体会.     

羊肚菌对大强度耐力运动大鼠肝组织自由基代谢和糖储备的影响

目的：研究羊肚菌对大强度耐力运动大鼠肝组织自由基代谢与糖储备的影响.方法：24只雄性SD大鼠随机均分为安静对照组、运动对照组、运动加药组.后两组在动物实验跑台上进行8周大强度耐力运动,运动加药组每日按350 mg/kg体重的剂量灌胃羊肚菌粉混悬液,而前两组灌胃同等体积蒸馏水.8周后,分别检测各组大鼠肝组织中SOD、GSH-Px、CAT、MDA、血清酶GPT、血糖、肌糖原、肝糖原等指标.结果：大强度耐力运动引起大鼠肝组织抗氧化酶SOD活性下降（P<0.05）,GSH-Px、CAT活性下降（P<0.01）,脂质过氧化产物MDA含量和血清酶GPT活性上升（P<0.01）,血糖浓度与肌糖原含量降低（P<0.01）,肝糖原含量降低（P<0.05）;与运动对照组相比较,补充羊肚菌使大强度耐力运动大鼠肝组织抗氧化酶SOD、GSH-Px活性上升（P<0.05）,CAT活性上升（P<0.01）,脂质过氧化产物MDA含量和血清酶GPT活性下降（P<0.01）,血糖浓度、肌糖原含量上升（P<0.01）,肝糖原含量上升（P<0.05）.结论：补充羊肚...     

Cocktail探针法 评价牛樟芝醇提物对人CYP450酶活性的影响

目的:研究牛樟芝醇提物对人肝CYP450酶的影响.方法:建立HPLC方法,通过Cocktail探针检测樟芝醇提物对人CYP450酶的影响.结果:牛樟芝各剂量组对CYP3A4/5有抑制作用;低剂量组对CYP2E1有促进作用,中、高剂量对CYP2D6、1A2、2E1、2C9亚型作用具有促进作用.结论:牛樟芝醇提物能促进人C...     

肝内胆管结石并肝门部胆管狭窄的外科治疗

目的：探讨肝内胆管结石并肝门部胆管狭窄的外科治疗．方法：回顾性总结本院1995年1月～2003年6月治疗肝内胆管结石并肝门部胆管狭窄54例的临床经验．结果：修复手术类型：用脐静脉修复狭窄占6例;用高位胆管狭窄切开整形、胆管空肠吻合术修复者占43例;用皮下通道型空肠肝门胆管成型术修复占5例．其中2l例行肝部分切除术．54例均得到随访,随访率100％,随访1～7a,平均3．3a．总优良率83．3％(45／54)。残石率5．6％(3／54),并发症发生率为11．1％,疗效满意．结论：充分显露肝门部胆管并解除胆管狭窄,合理地选择手术方式,彻底清除肝内结石及相应病灶并结合术后综合治疗,可提高治愈率．     

我院教职工腹部B超体检结果分析

重庆教育学院卫生科对450名教职工进行了腹部 B 超体检,分析体检结果发现,肝脾大、胆道结石及实质性脏器占位病变均以老年组发病率最高。本院胆道结石发病率9.8%,与重庆交通学院庹氏报道接近,而明显高于重庆建筑高等专科学校吴氏的报道,且以40岁以上、女性、高血脂、肥胖者为主。     

“木通”辨析

“木通”辨析@牟英     

辽东楤木对过度训练大鼠肝脏氧化损伤的预防作用

目的:以大鼠因过度训练而造成的机体损伤为模型,观察辽东楤木提取物对大鼠肝组织脂质过氧化、超氧化物歧化酶(SOD)活性和血清谷丙转胺酶(GPT)活性的影响。方法:将雄性Wistar大鼠随机分4组,即安静对照组(A)、运动组(B)、楤木低剂量加运动组(D)、楤木高剂量加运动组(E)。将大鼠按训练计划进行6周的游泳训练,并对D、E组分别灌服低、高剂量辽东楤木提取物,最后测定MDA含量、GPT活性及SOD活性。结果:过度训练后大鼠肝组织MDA含量和血清GPT活性显著上升(P<0.05),肝组织中SOD活性显著下降(P<0.05),而低剂量楤木提取物可显著抑制这种趋势的发生(P<0.05)。高剂量楤木提取物的作用效果不明显。结论:低剂量辽东楤木提取物对过度训练后大鼠肝脏的氧化损伤具有一定的预防作用。     

A novel way of liver preservation improves rat liver viability upon reperfusion

Background/aim： Currently, the liver is cold-preserved at 0-4 ℃ for experimental and clinical purposes. Here, we investigated whether milder hypothermia during the initial phase of the preservation period was beneficial for liver viability upon reperfusion. Methods： In the first set of experiments, rat livers were preserved either conventionally in clinically used histidine-trypthopan-ketoglutarate （HTK） solution （Group A： 45 min and Group B： 24 h） or by slow cooling HTK solution （from 13 ℃ to 3 ℃） during the initial 45 min of preservation （Group C： 24 h）. In the second set of experiments, additional groups of livers were evaluated： Group BB-preservation according to Group B and Group CC-preservation according to Group C. Further, some livers were preserved at 13 ℃ for 24 h. Livers were then reperfused using a blood-free perfusion model. Results： Bile production was approximately 2-fold greater in Group C compared to Group B. Alanine transaminase （ALT） and aspartate transaminase （AST） release into perfusate were 2-3-fold higher in Group B compared to Group C. No significant differences were found in ALT and AST release between Group C and Group A. Livers in Group CC compared to Group BB exhibited significantly lower portal resistance, greater oxygen consumption and bromosulfophthalein excretion into bile and lower lactate dehydrogenase （LDH） release into perfusate. Histological evaluation of tissue sections in Group BB showed parenchymal dystrophy of hepatocytes, while dystrophy ofhepatocytes was absent in Group CC. Livers preserved at 13 ℃ for 24 h exhibited severe ischemic injury Conclusion： These results suggest that the conventional way of liver preservation is not suitable at least for rat livers and that slow cooling of HTK solution during the initial phase of cold storage can improve liver viability during reperfusion.