肿瘤坏死因子、内皮素和一氧化氮在肝硬化大鼠门静脉高压高动力循环综合征中作用的研究

目的 了解肿瘤坏死因子（TNF）、内皮素（ET）和一氧化氮（NO）在门静脉高压高动力循环综合征（HCS）中的作用和地位以及门静脉血中含量的高低对HCS的影响。方法 四氯化碳诱导肝硬化大鼠在用抗TNF抗体，一氧化氮合成酶（NOS）抑制剂N^G－甲基－L－精氨酸处理前后测定门脉血TNF，ET和NO含量及肝组织NOS活性，同时监测血流动力学。结果 肝硬化大鼠门脉血中TNF，NO水平显著增高，ET也有轻度上升，肝组织NOS活性显著增高。在注射抗TNF抗体后，门脉血中TNF含量显著下降至对照水平，ET水平无变化，肝组织NOS活性较处理前下降15％－30％，同时HCS部分缓解。在注射N^G-甲基－L－精氨酸后，门脉血NO含量及肝组织NOS活性显著降低至对照水平，HCS明显缓解，门脉压力降至正常范围。结论 NO在HCS形成中起关键作用，TNF可能通过激活NOS使NO升高而发挥作用，ET与HCS形成无直接因素关系。     

门静脉部分结扎后大鼠血肿瘤坏死因子和内皮素与高动力循环综合征的关系

目的 探讨肿瘤坏死因子和内皮素在高动力循环综合征（HCS）形成中的作用。方法 门静脉部分结扎大鼠形成稳定的HCS后,检测用抗肿瘤坏死因子抗体处理前后各组的门静脉血肿瘤坏死因子及内皮素含量,同时检测血流动力学。结果 门静脉部分结扎后0．5h,大鼠门静脉血肿瘤坏死因子含量无变化,24h则显著增高,此后保持升高状态,并与HCS启动的时间相一致;门静脉血内皮素含量在门静脉部分结扎后各时相均有轻度升高。在注射抗肿瘤坏死因子抗体后,门静脉血肿瘤坏死因子含量明显降低至对照水平,内皮素含量无变化,HCS有部分缓解。结论 肿瘤坏死因子可能与HCS的启动有关,可能是维持HCS的媒介;内皮素与HCS形成无直接因果关系,可能是对血管张力失常的一种反应。     

一氧化氮在梗阻性黄疸大鼠肝、肾、肠组织中含量变化及意义

目的 了解一氧化氮（NO）在梗阻性黄疸大鼠肝，肾，肠组织中含量变化及意义。方法 大鼠胆总管结扎后，分别于第一周内和第三周内变化Aminoguanidine(AG)抑制NO合成，同时应用生理盐水（NS）作对照，检测不同时段抑制NO合成后大鼠肝，肾，肠组织中NO和丙二醛（MDA）含量，肌酐清除率（Ccr)，血清总胆红素（T－BIL）和丙氨酸氨基转移酶（ALT）含量及肠系膜淋巴结细菌移位（BT）率的变化。结果 胆总管结扎后，大鼠肝，肾，肠组织中NO含量明显升高，在胆总管结扎第一周抑制NO合成后，肝，肾肠组织中NO含量明显下降，MDA含量明显升高，血ALT明显升高，Ccr明显下降，肠系膜淋巴结BT率明显升高；而在胆总管结扎第三周抑制NO合成后，肝，肾，肠组织中NO和MDA含量明显下降，血ALT明显下降，Ccr明显升高，肠系膜淋巴结BT率明显下降。结论 NO在胆道梗阻引起的肝，肾，肠粘膜屏蔽功能障碍的发生机制中具有重要作用，既有保护作用，又有损害作用。梗阻早期表现为对组织的保护作用，后期表现为对组织的损害作用。     

一氧化氮在梗阻性黄疸大鼠肝、肾、肠组织中含量变化及意义

目的 了解一氧化氮（NO）在梗阻性黄疸大鼠肝、肾、肠组织中含量变化及意义。方法 大鼠胆总管结扎后,分别于第一周内和第三周内应用Aminoguanidine（AG）抑制NO合成,同时应用生理盐水（NS）作对照,检测不同时段抑制NO合成后大鼠肝、肾、肠组织中NO和丙二醛（MDA）含量、肌酐清除率（Ccr）血清总胆红素（T-BIL）和丙氨酸氨基转移酶（ALT）含量及肠系膜淋巴结细菌移位（BT）率的变化。结果 胆总管结扎后,大鼠肝、肾、肠组织中NO含量明显升高,在胆总管结扎第一周抑制NO合成后,肝、肾、肠组织中NO含量明显下降,MDA含量明显升高,血ALT明显升高、Ccr明显下降、肠系膜淋巴结BT率明显升高;而在胆总管结扎第三周抑制NO合成后,肝、肾、肠组织中NO和MDA含量明显下降,血ALT明显下降、Ccr明显升高。肠系膜淋巴结BT率明显下降。结论NO在胆道梗阻引起的肝、肾、肠粘膜屏障功能障碍的发生机制中具有重要作用,既有保护作用,又有损害作用。梗阻早期表现为对组织的保护作用,后期表现为对组织的损害作用。     

阻塞性黄疸时L-精氨酸对肾功能的保护作用

目的：研究阻塞性黄疸（OJ）时，L－精氨酸（L－Arg)对肾功能的保护作用。方法：胆总管结扎大鼠30只，随机分成生理盐水对照（NS）组、L－精氨酸（L－Arg)组和L－硝基精氨酸（L－NNA）组，每组10只。胆总管结扎后第2天起分别腹腔注射1ml NS、1ml L-Arg(500mg/kg)、1ml L-NNA(10mg/kg)，连用9d；假手术（SO）组用1ml NS腹腔注射。观察各组肾功能的变化，同时测定血和肾组织内皮素（ET）、一氧化氮（NO）水平、一氧化氮合酶（NOS）活性和丙二醛（MDA）的含量。并用图像分析检测ET1 mRNA和NOS mRNA表达的部位及量的变化。结果：用L－Arg后，血和肾组织NOS活性增加，肾组织ET1 mRNA表达减少，血和肾组织ET下降，NO升高；同时伴有内生肌酐清除率（Ccr)、肾皮质平均血流（RCBF）的升高，肾组织MDA含量降低。结论：L－Arg通过增强血和肾组织NOS活性来增加体内NO水平、抑制ET1 mRNA表达、降低体内ET水平，从而提高Ccr与RCBF，减轻阻塞性黄疸时的肾功能损伤。     

总抗氧化能力和一氧化氮合酶对大鼠隐睾生殖细胞凋亡的影响

目的：探讨总抗氧化能力（T－AOC）和一氧化氮（NO）合物（NOS）对隐睾生殖细胞凋亡的影响。方法：SD雄性大鼠日龄22d时复制单侧隐睾模型。用生物素－dUTP/酶标亲和素测定法检测睾丸生殖细胞凋亡；用硝酸还原酶法测定睾丸组织中NO含量；用化学比色法测定睾丸组织中T－AOC、NOS活性。结果：术后第7天，与对侧睾丸相比，隐睾发生凋亡的生殖细胞数显著增加，NO含量及NOS活性显著上升（P＜0．01），在隐睾组织中两者呈正相关（γ3=0.890,P＜0．01）；T－AOC显著降低（P＜0．01）。结论：隐睾组织中NO和NOS升高、T－AOC下降是隐睾生殖细胞凋亡增加的生化机制之一。     

一氧化氮在大鼠异种肝移植急性排异中的作用及其黄递酶组化研究

目的：探讨一氧化氮（NO）在肝移植急性反应中的功能作用及NO合酶 （NOS）的细胞定位。方法：应用金黄地鼠至大鼠异种原位肝移植急性排斥及大鼠同基因原位肝移植动物模型,观察L－NMMA对受体存活期,ALT,TGF-α及移植肝的病理影响。应用NADPH－d组化染色观察NOS的活性及其细胞来源,结果：表明L－NMMA可明显降低异种肝移植受体存活期,加剧其肝功能恶化、上调TGF-α、加剧移植肝的病理损害、异种肝移植组NADPH－d组化染色呈强阳性,主要在肝实质细胞及浸润炎性细胞表达,结论：NO在大鼠肝移植急性排斥反应中可能具有重要的免疫保护作用。     

烧伤大鼠小肠组织中两型一氧化氮合酶变化的观察

目的 研究烧伤后大鼠小肠组织中两型一氧化氮合酶的变化及与一氧化氮(NO)的关系。方法 采用30％TB-SAⅢ度烧伤大鼠模型,分别检测了小肠组织中NO含量及原生型NOS(cNOS)和诱导型NOS(iNOS)的活性,并分析了NO的变化规律及其与两型NOS之间的关系。结果 烧伤后小肠组中iNOS活性大幅上升,与NO的变化趋势一致,二者呈显著正相关(P<0.01),而cNOS活性呈下降趋势,与NO相关不显著(P<0.05)。结论 烧伤后小肠组织中NO的变化主要受iN-OS活性影响,iNOS活性上升,cNOS活性下降可能与烧伤后胃肠道病理变化密切相关。     

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。     

冠状动脉旁路术围术期肺动脉血浆一氧化氮合成酶活性与一氧化氮浓度的变化

目的 研究冠状动脉旁路术围术期肺动脉血浆一氧化氮合成酶（NOS）活性和一氧化氮（NO）浓度的变化。方法 选择30例冠状动脉旁路手术（CABG）病人,在围术期抽取肺动脉血测定NOS和NO值。结果 肺动脉血浆中NOS和NO水平虽有明显变化（P＜0．05）,但NO浓度与NOS活性的增减并不一致：当NOS活性降低时,NO浓度增高;反之当NOS活性显著增高时,NO浓度降低。结论 在行CABG围术期中,肺动脉血浆中内源性NO分泌无法满足应激时自身保护对其的需要。     

Beware the Anomalous Portal Vein

Portal vein thrombosis is an unusual potential complication of liver resection. In our case it was due to ligation of the right branch of the portal vein during right hepatectomy in a patient without portal vein bifurcation. Hepatic angiography can delineate this abnormality and influence the choice of surgical management.     

Portal Vein Pull-Through Technique and Thrombectomy for Extensive Portal Vein Thrombosis

BackgroundHerein, a different technique is presented describing complete dissection of the entire portal vein (PV), superior mesenteric vein (SMV), and splenic vein, thus enabling a complete thrombectomy without the risk of uncontrolled hemorrhage due to blind thrombectomy.MethodsIn cases where a thrombectomy would not be an option because of extensive thrombosis involving the confluence of the PV and SMV, small branches of the SMV, including the inferior mesenteric vein, were divided. Both the SMV and splenic vein were encircled separately. Then, the side branches of the PV above the pancreas, left gastric vein on the left side, and superior pancreatoduodenal vein on the right side were divided. The lateral and posterior part of the PV were dissected within the pancreas both from above and below, allowing the main PV completely free from attachments. At this point, the splenic vein and SMV were clamped, and the main PV was divided above the pancreas and then pulled back through the pancreatic tunnel. The thrombus was easily dissected of the vein under direct visualization, and afterward the PV was redirected to its original position. Then, the liver transplant was carried out in a regular fashion.ResultsThis technique was applied to 2 patients. The first was a 43-year-old man who underwent a right lobe living donor liver transplant because of hepatitis B virus–related cirrhosis. The patient is still alive and well with stable liver function after 15 years of follow-up. The second was a 69-year-old woman who underwent a right lobe living donor liver transplant because of hepatitis C virus and hepatocellular carcinoma. She survived the procedure and her liver function was entirely normal afterward. She died of pneumonia and sepsis 5 months after transplant.ConclusionsThis technique enables complete dissection of the entire PV, SMV, and splenic vein. Thus, complete thrombectomy under direct visualization without the risk of uncontrolled hemorrhage can be performed.     

门静脉癌栓与血栓的超声造影研究

目的探讨超声造影对门静脉癌栓和血栓的鉴别诊断价值。方法应用超声造影剂（SonoVue）对16例门静脉癌栓及8例门静脉血栓行实时低机械指数超声造影，观察并分析其造影增强特征。结果16例癌栓超声造影动脉相10例呈整体均匀性增强，2例呈整体不均匀性增强，2例呈整体轻度增强，2例栓子一部分增强，另一部分无增强；门脉相特别是门脉相晚期和延迟相14例栓子呈充盈缺损状态，2例栓子仍呈轻微强化。4例常规彩超检查未能检出动脉血流信号而不能确诊的癌栓．超声造影均显示其动脉相增强。8例血栓行超声造影后整个造影过程栓子均未见增强。结论超声造影可敏感地反映门静脉栓子的血流灌注，门静脉癌栓和血栓在超声造影后有显著的特征，有助于两者的鉴别诊断。     

Portal Vein Thrombosis After Hepatectomy

Background

Although various complications after hepatectomy have been reported, there have been no large studies on postoperative portal vein thrombosis (PVT) as a complication. This study evaluated the incidence, risk factors, and clinical outcomes of PVT after hepatectomy.

Methods

The preoperative and postoperative clinical characteristics of patients who underwent hepatectomy were retrospectively analyzed.

Results

A total of 208 patients were reviewed. The incidence of PVT after hepatectomy was 9.1 % (n = 19), including main portal vein (MPV) thrombosis (n = 7) and peripheral portal vein (PPV) thrombosis (n = 12). Patients with MPV thrombosis had a significantly higher incidence of right hepatectomy (p < 0.001), larger resection volume (p = 0.003), and longer operation time (p = 0.021) than patients without PVT (n = 189). Multivariate analysis identified right hepatectomy as a significant independent risk factor for MPV thrombosis (odds ratio 108.9; p < 0.001). Patients with PPV thrombosis had a significantly longer duration of Pringle maneuver than patients without PVT (p = 0.002). Among patients who underwent right hepatectomy, those with PVT (n = 6) had a significantly lower early liver regeneration rate than those without PVT (n = 13; p = 0.040), and those with PVT had deterioration of liver function on postoperative day 7. In all patients with MPV thrombosis who received anticoagulation therapy, PVT subsequently resolved.

Conclusions

Postoperative PVT after hepatectomy is not rare. It is closely related to delayed recovery of liver function and delayed liver regeneration.     

Portal Decompression Using the Inferior Mesenteric Vein

We report five patients with variceal hemorrhage, in three cases secondary to diffuse thrombosis of the portal, superior mesenteric and splenic veins. Mesenteric angiography demonstrated patency of the inferior mesenteric vein (IMV) in each, and successful portal decompression by anastomosis of the IMV to the left renal vein (n=4) or the inferior vena cava (n=1) was accomplished. Bleeding was permanently controlled: four patients have survived from one to eight years post-operatively. Because shunt procedures utilizing the IMV are technically straightforward, subtotally decompress the portal system and avoid the right upper quadrant, they may be advantageous in certain clinical settings.     

Portal Vein Stenting to Treat Portal Vein Stenosis in a Patient With Malignant Tumor and Gastrointestinal Bleeding

This report describes the successful use of portal venous stent placement for a patient with recurrent melena secondary to jejunal varices that developed after subtotal stomach preserved pancreatoduodenectomy (SSPPD). A 67-year-old man was admitted to our hospital with tarry stool and severe anemia at 2 years after SSPPD for carcinoma of the head of the pancreas. Abdominal computed tomography examination showed severe stenosis of the extrahepatic portal vein caused by local recurrence and showed an intensely enhanced jejunal wall at the choledochojejunostomy. Gastrointestinal bleeding scintigraphy also revealed active bleeding near the choledochojejunostomy. Based on these findings, jejunal varices resulting from portal vein stenosis were suspected as the cause of the melena. Portal vein stenting and balloon dilation was performed via the ileocecal vein after laparotomy. Coiling of the jejunal varices and sclerotherapy of the dilate postgastric vein with 5% ethanolamine oleate with iopamidol was performed. After portal stent placement, the patient was able to lead a normal life without gastrointestinal hemorrhage. However, he died 7 months later due to liver metastasis.Key words: Portal vein stenosis, Portal vein stent, PancreatoduodenectomyObstruction of the extrahepatic portal vein can lead to portal hypertension, splenomegaly, and gastrointestinal bleeding due to esophageal or gastric varices. Malignant portal vein stenosis accounts for 15 to 24% of all cases of portal venous stenosis or occlusion and usually results from portal vein tumor thrombus or external compression of the portal vein by neoplasms.^1–4 When a patient with malignant tumors undergoes subtotal stomach preserved pancreatoduodenectomy (SSPPD), formation of hepatopetal collaterals is precluded by lymph node dissection and resection of the peribiliary vascular plexus around the hepatoduodenal ligament. Instead, jejunal varices form at the choledochojejunostomy site. The treatment of portal vein stenosis remains controversial, and the indications for portal vein stent placement have not yet been clarified.This report describes a case of successful portal vein stenting for a patient with portal vein stenosis and repetitive bleeding from jejunal varices that developed after SSPPD.