良性梗阻性黄疸患者血清中IGF-1变化的意义

目的探讨梗阻性黄疸对肝脏分泌胰岛素样生长因子1(IGF1)的影响。方法收集20例梗阻性黄疸患者的临床资料,并对患者血清TNFα、肝功能指标(ALT、ALP、TB)、内毒素(ET)及IGF1进行检测。结果良性梗阻性黄疸患者与单纯胆囊结石患者相比,IGF1明显降低(P<0.01),而ET、TNFα、ALT、ALP及TB均明显升高(P<0.01);在胆道梗阻解除后,IGF1明显上升,ET、TNFα、ALT、ALP及TB则明显下降(P<0.01)。在良性梗阻性黄疸时,血清中IGF1浓度的变化与ET的浓度变化呈负相关(r=-0.761,P<0.01)。结论梗阻性黄疸时,内毒素血症可影响肝脏分泌IGF1,而IGF1则可以作为判断梗阻性黄疸时肝脏功能改变的指标。     

降低高位胆道梗阻病人再手术率的手术前努力

高位胆管梗阻是指总肝管及其以上的胆管梗阻。良性高位胆管梗阻是胆石、胆管狭窄及其引起的胆管炎等因素引起的梗阻 ;其次是损伤性肝门部胆管闭塞或狭窄引起的梗阻 ;其它较少见原因如先天性胆道狭窄或闭锁、原发性硬化性胆管炎、放射损伤等因素均可引起高位胆管梗阻或全程胆管狭窄和梗阻。高位胆管梗阻由于病变位置深 ,相邻结构复杂 ,常引起黄疸、发热、肝内感染、脓肿形成、肝内胆道出血、胆汁性肝硬化、门静脉高压等并发症 ,造成临床处理困难。因此 ,术前必须充分检查和准备 ,以期获得较好的手术效果。一、详细了解病史和既往治疗经过高位…     

内毒素引起阻塞性黄疸大鼠肾功能障碍的机制

目的 探讨阻塞性黄疸(obstructive jaundice,OJ)时内毒素引起肾功能障碍的机制.方法 SD大鼠60只,胆总管结扎后,分5 d(B1),10 d(B2),15 d(B3)三组,每组各10只,同时建立相应对照组(A1,A2,A3),另30只胆总管结扎后分3组(SHUD,LAC,NS),每组各10只,分别用2 ml舒胆合剂、乳果糖液、生理盐水灌胃,连用9 d.观察内毒素、血和肾组织中内皮素(endothelin,ET)、一氧化氮(nitric oxide,NO)的含量、一氧化氮合酶(nitric oxide synthase,NOS)活性及肝、肾功能的变化.结果 血内毒素与血、肾组织ET含量,ET/NO比值呈显著正相关(P＜0.05,r=0.630,0.438,0.496,0.453),与肌肝清除率(creatinine clearance,Ccr)和肾皮质血流量(renal cortical blood flow,BCBF)呈显著负相关(P＜0.05,r=-0.600,-0.410).血、肾组织ET/NO比值与Ccr,RCBF呈显著负相关(P＜0.05,r=-0.449,-0.558,-0.626,-0.731).血和肾组织内NO水平与内毒素水平呈负相关(P＜0.05,r=-0.518,-0.441),与Ccr、RCBF呈正相关(P＜0.05,r=0.422,0.496,0.400,0.659).SHUD组与LAC血内毒素、ET水平组明显降低,血和肾组织NO,NOS活性以及Ccr,RCBF较NS组明显升高.结论 OJ时内毒素可通过刺激ET的释放,提高ET/NO比值,使肾内缩血管因子与扩血管因子比例失调而损伤肾功能.     

一氧化氮、内皮素和内毒素与肝硬化腹水及肝功能

目的：测定不同阶段肝硬化患者血浆的一氧化氮（NO），内皮素（ET）及内毒素水平，探索它们对肝硬化腹水形成和肝功能损害所起的作用及其相互关系。方法：测血浆NO的代谢产物NO2^-浓度（Griess法），ET－1浓度（放免法），内毒素浓度（鲎试验的显色基质法）及肝功能。结果：（1）血浆NO、ET及内毒素浓度在肝硬化各组均明显高于正常对照组，在有腹水组明显高于无腹水组；（2）血浆NO、ET、内毒素水平随肝功能损害加重逐渐升高；（3）肝硬化患者血浆内毒素与NO、ET水平分别呈正相关，NO与ET水平呈正相关，结论：血浆内毒素、NO和ET升高可能在肝硬化病程进展中起了重要作用，是形成腹水的重要因素，三者相互依赖、相互影响的协同作用是肝硬化进展的重要机制之一。     

恶性梗阻性黄疸胆囊癌导致胆道梗阻的外科治疗

胆囊癌侵袭能力强,就诊时有20％～40％出现黄疸,在晚期胆囊癌黄疸发生率高达90％。梗阻性黄疸是胆囊癌较突出的临床问题,这种恶性胆管梗阻如不能解除,常由于进行性胆道梗阻并胆管炎致肝功能衰竭而加速死亡,预后很差。因此对于胆囊癌并胆道梗阻的病人应持积极的治疗态度,即使不能做到治愈性切除、姑息性手术,也应解决胆道梗阻性黄疸所导致的肝损害和全身性影响,从而提高病人的生存质量。     

胆石病员一氧化氮和内皮素的变化及其意义

探讨胆囊结石,胆石伴梗阻性黄疸时ＥＴ－１、ＮＯ变化及其临床意义。方法：前瞻性比较观测正常人、胆囊结石、胆石并黄疸病员血液ＮＯ、ＥＴ－１及肝功能指标。结果胆石并黄疸组：ＮＯ、白蛋白、球蛋白、ＡＬＴ、血清胆红素和另两组比较,有显著判别与ＥＴ－１、ＡＬＴ呈负相关。     

内皮素、一氧化氮与阻塞性黄疸肾功能障碍关系的实验研究

目的 研究内皮素(Endothelin ET)、一氧化氮(Nitric Oxide NO)与阻塞性黄疸(Obstructive Jaundice OJ)肾功能障碍的关系。方法 雄性SD大鼠胆总管结扎后随机分成5天、10天、15天三组，同时建立对应的假手术对照组。观察肾功能的变化，同时测定血和肾组织ET、NO水平及一氧化氮合酶(Nitric Oxide Synthetase NOS)活性，并用图像分析检测ET—1mRNA和NOS—mRNA表达的部位和量的变化。结果 随胆总管梗阻时间的延长，血和肾组织ET升高，NO下降，ET／NO比值与内生肌酐清除率(Creatinine clearance rate Ccr)、肾皮质血流(Renal cortex blood flow RCBF)呈负相关。肾组织ET—1mRNA和iNOS mRNA表达增加，血和肾组织NOS活性降低。结论 血和肾组织ET升高，NO下降，ET／NO比值升高是导致OJ时肾功能损伤的原因之一。     

胆道梗阻后心脏损害的研究

目的　探讨胆道梗阻后心脏损害及损害机制。方法　分动物及临床实验 ;胆道结扎并离断 ,大鼠行颈动脉插管测心率、血压、心输出量 ,动态观测心肌组织丙二醛 (MDA )和超氧化物歧化酶 (SOD)、血清总胆红素 (TBil)、胆汁酸 (TBA)、内毒素 (ET)、肿瘤坏死因子 (TNFα)含量 ,ABC免疫组化法定位 TNFα在心肌组织中的表达和分布。临床以放射性同位素对胆道梗阻病人行心血池显像 ,得出左心室功能参数。结果　胆道梗阻后大鼠血压、平均动脉压、心输出量下降 ,血清 TBil、TBA、ET、TNFα、心肌组织 MDA逐渐升高 ,SOD逐渐减少 ,胆道梗阻组与对照组比较 ,P<0 .0 5 ,心肌组织 MDA含量与血清 TNFα含量变化呈正相关 ,r值分别为 0 .932和 0 .85 0 ,光电镜检查心肌组织细胞 ,随胆道梗阻时间延长损害加重。胆道梗阻组病人局部射血分数 REF3和 REF4、轴缩短率 RS3和 RS4明显低于对照组。结论　胆道梗阻后心脏功能受损且随黄疸加深而损害加重 ,自由基损伤、内毒素血症、TNFα等细胞因子的综合作用是胆道梗阻所致心脏损害的重要机制     

恶性梗阻性黄疸的姑息性减黄治疗

恶性梗阻性黄疸（Malignant obstructive jaundice,MOJ）是指因恶性肿瘤如胰头癌、胆管癌、胆囊癌、十二指肠肿瘤或壶腹部肿瘤压迫或阻塞肝外胆道而导致的黄疸.MOJ由于黄疸出现时肿瘤多数已进入晚期阶段,大部分患者已失去根治性手术机会.但是,如果不尽早解除胆道梗阻,患者往往在短期内死于肝功能衰竭或胆管炎,因此对于晚期已失去根治性机会的患者应尽早采取姑息性手段解除胆道梗阻,避免黄疸进一步加重,预防肝功能进行性恶化,从而延长患者生存期、提高生活质量.术式选择的总体原则是尽可能符合生理,常见的姑息性胆道引流术包括手术引流、经内镜胆道引流和经皮肝穿刺胆道引流,每种方法各有利弊.本文就MOJ的诊断和各种姑息性减黄治疗方法作一简单阐述.     

梗阻性黄疸术后肝内胆汁淤积症的病因及治疗体会

目的 探讨梗阻性黄疸术后肝内胆汁淤积症的病因和治疗方法.方法 226例梗阻性黄疸经手术解除胆道梗阻后1～14 d内发生的28例肝内胆汁淤积症的病因,在积极抗感染、保肝治疗的基础上,辅以肾上腺糖皮质激素冲击治疗.结果 28例中,胆道感染合并内毒素血症22例(78.6％),围手术期出现一过性低血压5例(17.9％),术后HBV-DNA阳性9例(32.1％),均明显高于正常治愈组(P＜0.05或P＜0.01).经以上方法治疗后27例在术后1～2个月血清胆红素、丙氨酸转氨酶逐渐下降至正常,肝功能明显改善,1例因癌症晚期多器官功能衰竭死亡,治愈率96.4％.结论 梗阻性黄疸术后肝内胆汁淤积症的原因可能为胆道感染、内毒素血症、缺血再灌注损伤、肝细胞乙型肝炎病毒活动等,治疗方面以肾上腺糖皮质激素冲击疗法及腺苷蛋氨酸等护肝治疗有效.     

一氧化氮、内皮素-1在内毒质所致肝脏损伤中的作用机制研究

目的 探讨一氧化氮（NO）和内皮素-1（ET-1）在内毒素所致肝脏损伤中的作用机制。方法 Waster大鼠40只随机分成对照组，内毒素组、内毒素组、内皮素受体拮抗剂组和左旋精氨酸组，观察各组大鼠血浆NO和ET-1水平，肝脏功能变化，在光镜下观察肝细胞损伤程度，在电镜下观察肝脏超微结构改变。结果 大鼠投予内毒素12h后，血浆NO和ET-1水平明显下升，血浆转氨酶水平增加，肝细胞明显水肿，变性和坏死，肝筛的数量和直径明显减少，左旋精氨酸和内皮素受体损坏抗剂均能明显减轻肝脏功能和结构的损伤，结论 在内毒素所致肝损伤中，NO起保护性作用，而ET-1则起促进作用，二者在肝脏中的作用可能是通过作用于肝筛而引起的。     

A research on the cholestasis caused by continuous endotoxemia

Intrahepatic cholestasis is often observed in patients without obstruction of the bile duct, who are suffering from severe prolonged infection in the field of peptic surgery. Clinical data were analyzed in recently experienced 18 cases which showed this kind of jaundice. In those case, high rates of endotoxemia and high rates of gram negative bacilli were seen. This fact made us infer that endotoxins might cause jaundice. In order to clarify the mechanism of the jaundice, we made an experimental model of persistent endotoxemia in rats. Low-dose endotoxin was infused continuously to Donryu-rats and bile-output was observed with external bile-guiding tube for 24 hours. In the endotoxin group, bile-output was significantly decreased whereas it was not changed in the control group. In addition, serum bilirubin was elevated in the endotoxin group, whereas it did not change in the control group. Blood-flow of liver tissue and systemic arterial blood pressure did not show any severe decrease under the continuous endotoxemia. Data of bile-output and bile acid showed bile acid independent flow might be depressed by endotoxin infusion. This model was thought to be under non-shock condition and useful to investigate jaundice seen in patients under continuous endotoxemia.     

内毒素血症与梗阻性黄疸病人肾功能损害的关系

目的: 探讨梗阻性黄疸(梗黄)病人血浆内毒素(ET)水平与肾功能的关系.方法: 动态观察30例梗黄(梗黄组)手术前后血浆ET、肌酐(Cr)、尿素氮(BUN)含量及内生肌酐清除率(Ccr)变化,并与21例无黄疸病人(对照组)进行同步比较.结果: 梗黄组外周血ET水平显著升高(P<0.01),Ccr显著降低(P<0.01);门静脉血ET水平又显著高于外周血(P<0.05),术后5 d内ET水平降低不明显;术后第1天ET反而升高(P<0.05),Ccrr更趋下降(P<0.05),并伴有血Cr、BUN升高(P<0.05);5 d后随ET水平逐渐下降,Cor逐步上升,第15天ET、Ccr两项指标接近正常水平;ET与Ccr呈显著负相关(r=-0.55,P<0.05).对照组血浆ET呈低水平,Ccr在100ml/min左右,手术前后变化均不显著(P>0.05).结论: 肠源性内毒素血症是梗黄肾功能损害的重要原因,围手术期以手术后一周内最为严重.     

精氨酸对梗阻性黄疸病人肾脏损害的保护作用

目的 观察精氨酸对梗阻性黄疸（梗黄）病人肾功能的保护效应。方法34例梗黄病人,随机分为两组,分别在术前给予一般治疗（梗黄组）和精氨酸治疗（治疗组）,连续治疗7d,观察手术前后血ET（内毒素）及Ccr（内生肌酥清除率）变化,并与20例无黄疸的慢性胆囊炎、胆囊结石病人（对照组）比较。结果（1）入院时梗黄组与治疗组外周血ET及Ccr水平比较,差别无显著意义（P>0.05）,但上述两组ET均显著高于对照组（P<0.01）,Ccr显著低于对照组（P<0.01）;（2）梗黄组术后第1天血ET较术前升高（P<0.05）,Ccr更趋下降（P<0.05）,7d后随血ET水平下降,Ccr逐渐升高,第14天ET和Ccr两项指标接近正常水平;ET与Ccr呈显著负相关（P<0.05）;（3）治疗组用药后血ET水平下降,术后保持较低水平,而Ccr用药后升高,第7天ET、Ccr两项指标已接近正常水平。结论 术前使用精氨酸可显著降低梗黄病人内毒素血症,提高内生肌酥清除率,对肾功能具有良好的保护作用。     

梗阻性黄疸患者的内毒素血症及其对机体的影响

４９例梗阻性黄疸（梗黄）患者（实验组）和８１例无黄疸胆系疾病患者（对照组）围手术期外周血的内毒素（ＥＴ）检测结果表明，实验组：①术前ＥＴ阳性率明显高于对照组（Ｐ＜０．００１）；②术后１０～１２天夹闭Ｔ／Ｙ管后ＥＴ阳性率明显低于术前和夹管前（Ｐ＜０．００１）；③伴急性化脓性胆管炎（ＡＣＳＴ）的患者ＥＴ阳性率明显高于无ＡＣＳＴ的患者（Ｐ＜０．００１）。作者认为，本组梗黄患者中出现的肾功能障碍、胃肠道出血以及２例患者的死亡，可能部分与内毒素血症有关。     

Study on mechanism of onset of endogenous endotoxemia during obstructive jaundice--with special reference to involvement of biliary infection

To clarify how biliary infections affect onset of endogenous endotoxemia during obstructive jaundice, I tried to review the clinical result of 104 cases of obstructive jaundice, and conducted a Limulus test of portal and peripheral blood in 20 cases of obstructive jaundice and an animal study using 38 rabbits. In cases of obstructive jaundice complicated by biliary infections, clinical improvement of jaundice became significantly unfavorable, and the outcome of surgical operation was significantly inferior to the cases without biliary infections. The endotoxin positive rate in the portal blood of obstructive jaundice was 65% (13 of 20 cases), among which 10 cases (79.6%) was also positive in the peripheral blood. Of these 10 cases, 7 cases manifested endogenous endotoxemia with no infectious focus, and prognosis of these cases was poor. The endotoxin positive rate in portal blood of obstructive jaundice group was also significantly higher than that of non-jaundice group in animal study, and when the reticuloendothelial system was blocked, the endotoxin positive rate in the peripheral blood showed an increasing tendency. In the animal group with experimental cholangitis, all the endotoxin positive animals in the portal blood were also positive in the peripheral blood. This result suggests that biliary infections accelerate a decrease in the reticuloendothelial function during obstructive jaundice. From these results, endogenous endotoxemia seems to affect the onset of various complications during obstructive jaundice and unfavorable prognosis.     

654－2对梗阻性黄疸内毒素致肾脏损害的临床干预

目的 :观察梗阻性黄疸 (梗黄 )患者内毒素 (ET)对肾功能影响以及 6 5 4 2的干预作用。方法 :30例梗黄患者 ,随机分为两组 ,分别给予一般治疗 (A组 )和 6 5 4 2治疗 (B组 ) ,观察手术前后血ET及内生肌酐清除率 (Ccr)变化 ,并与 2 1例无黄疸患者进行同步比较。结果 :(1)入院时A、B两组外周血ET及Ccr水平无显著差异 (P >0 0 5 ) ,但ET水平均显著高于对照组 (P <0 0 1) ,Ccr均显著低于对照组 (P <0 0 1)。 (2 )A组门静脉血ET水平显著高于外周血 (P <0 0 5 ) ,A组术后随ET水平下降 ,Ccr逐渐升高 ,第 15天ET和Ccr两项指标达到正常水平。ET与Ccr呈显著负相关 (r =- 0 5 9,P <0 0 5 )。 (3)B组用药后外周血和术中门静脉血ET水平均显著降低 ,术后保持较低水平 ,而Ccr用药后略有升高 ,术后继续上升 ,第 10天ET、Ccr两项指标达到正常水平。结论 :6 5 4 2可降低梗黄患者肠源性ET水平 ,对肾功能损害具有良好的保护作用。     

Endotoxemia after surgery in digestive diseases

The blood level of endotoxin after operations in patients with digestive diseases, mainly liver cirrhosis and obstructive jaundice, and the complications most likely related to the presence of endotoxemia were investigated. Twenty-seven patients without either liver cirrhosis or obstructive jaundice showed a minimal elevation of the endotoxin level in blood, as shown by 6.1 +/- 3.9 pg/ml at the first postoperative day and there was only one anastomotic leakage. On the other hand, 18 patients with liver cirrhosis showed a notable and persistent endotoxemia after surgery. The cirrhotic patients who especially underwent splenectomy and hepatectomy showed marked elevations of endotoxin level at the first postoperative day, with values of 151.0 +/- 46.1 pg/ml and 101.3 +/- 36.2 pg/ml, respectively, and one of these patients died of hepatic failure. Thirteen patients with obstructive jaundice developed endotoxemia evidenced by the value of 21.6 +/- 4.8 pg/ml at the first day after surgery. Among these patients, two had gastrointestinal bleeding and one developed DIC. The markedly high and persistent levels of endotoxin in patients with liver cirrhosis or obstructive jaundice may be possibly related with the development of MOF.     

Thromboxane as a possible hepatotoxic factor increased by endotoxemia in obstructive jaundice

In a study using rats, we investigated whether liver damage induced by endotoxemia in obstructive jaundice is associated with thromboxane (TX) in order to acertain whether its vasoconstrictive and platelet aggregating properties play a role in reducing liver blood flow. The rats were divided into the following 5 groups; a control group, an endotoxin (Et) group, a bile duct ligation (BDL) group, a bile duct ligation and endotoxin (BDL + Et) group and an OKY046 (Thromboxane synthetase inhibitor) treated bile duct ligation + endotoxin (OKY-BDL + Et) group. The blood TXB2 levels in the Et, BDL and BDL + Et groups were higher than those in the control group. The liver TXB2 levels in the Et and BDL + Et groups were also higher than those in the control group. Liver phospholipids and liver blood flow decreased in the BDL + Et group, whereas in the OKY-BDL + Et group they returned close to the control group levels by decreasing the TXB2 levels in both the liver and blood to normal. These results suggest that the high level of TX in the blood and liver tissue may further aggrevate the liver during endotoxemia in obstructive jaundice by inhibiting liver blood flow.