丹参与骨碎补注射液防治激素诱发股骨头坏死的实验研究

目的探讨丹参和骨碎补对激素性股骨头坏死的防治机理及其交互作用.方法选用家兔50只,随机分成五组:模型组、丹参组、骨碎补组、丹参 骨碎补组、对照组.8周后观察五组家兔血液流变学、脂代谢、股骨头组织学等指标的改变.结果与对照组相比,模型组股骨头疏松,易于凿切,血液粘度和血脂升高,骨小梁变细、稀疏,空骨陷窝率增高,髓腔脂肪细胞增多;而其余各组上述病变有不同程度的减轻,其中以丹参 骨碎补组病理改变最轻.结论①丹参、骨碎补均能预防激素所致的高粘滞血症和高脂血症;②骨碎补能提高血钙血磷,激活成骨细胞,提高股骨头的骨密度,能预防激素性骨质疏松;③两药在预防SANFH方面有协同作用.     

影响肝外伤手术死亡的危险因素分析

目的分析影响肝外伤手术死亡的危险因素,探讨其临床意义。方法根据AAST和ISS标准,回顾性分析90例肝外伤手术病例,对影响手术死亡的危险因素进行单因素比较和Logistic回归分析。结果死亡15例,其中Ⅲ级2例、Ⅳ级4例、Ⅴ级9例,总体手术死亡率17%。Ⅳ~Ⅴ级肝外伤手术方式的单因素比较提示:清创性肝切除术的相对危险度是0.73;而规则性肝切除术、肝静脉或肝后下腔静脉修补术相对危险度分别是1.32、1.52。Logistic回归分析提示:ISS分会和术中失血量是影响手术死亡率的2个独立因素。结论ISS分值、术中失出血量和手术方式是影响肝外伤手术死亡的3个重要因素,娴熟的手术技能和合理的手术方式可以减少术中出血量和降低手术死亡率。     

胃癌根治术中肝动脉变异及意义

目的介绍胃癌根治术时发现肝动脉变异情况。方法回顾性分析208例胃癌根治术时遭遇的肝动脉变异情况。结果208例中发现肝动脉变异3例,术中游离时注意保留肝脏、胆囊的血供分支。结论胃癌根治术时应注意肝动脉变异可能,避免损伤邻近器官的血供。     

无创伤法联合测定门静脉压力及肝血流评价肝硬化疗效

目的　为临床评价肝硬化疗效提供有价值的手段。方法　采用99Tcm-RBC及99Tcm-MIBI分别测定 16例肝硬化患者治疗前后的肝血流及门静脉压力。前者选择峰时 (T(max) 、半廊清时 (T1/ 2 )、廊清率 (K值 )及肝血流(LBF)等作为观察指标 ;后者以心 /肝 (H/L)比值及门静脉压力 (PVP)为观察指标。结果　治疗前Tmax、T1/ 2 、K值及LBF分别为 1.83± 1.0 4min、5 .3 7± 2 .19min、0 .10± 0 .0 3及 0 .45± 0 .16L/min ,而治疗后分别为 0 .86± 0 .2 0min、3 .80± 1.86min、0 .14± 0 .0 4及 0 .64± 0 .2 0L/min ,治疗前后各项指标均有非常显著性差异 (P <0 .0 1或 0 .0 0 1)。服药前H/L、PVP分别为 0 .73± 0 .16及 3 .0 0± 0 .5 5kPa;治疗后分别为 0 .47± 0 .18及 2 .2 0± 0 .62kPa,与治疗前相比均有非常显著性差异 (均P <0 .0 0 1)。结论　所用测定肝血流及门静脉压力的两种方法均无创伤性 ,用于观察肝硬化疗效有一定价值     

生长激素抗肝纤维化的作用及其机制

目的　探讨重组人生长激素 (rhGH)对肝硬化大鼠在肝功能、门静脉高压等方面的治疗作用及其可能的机制。方法　雄性SD大鼠建立肝硬化模型 ,随机分组 ,分别给予NS、rhGH (333ng/KgBW ,ip ,qd× 7d)处理。 结果　rhGH处理前后肝硬化肝组织GHR的配体结合容量 [fmol/mg ,(31± 4 )vs .(4 0± 7) ]及其mRNA量 (iOD ,pixel)均显著升高 (2 3± 3)vs.(4 2± 8) ;P <0 0 5 ,肝硬化大鼠血清白蛋白 (g/L )显著升高 (2 9± 4 )vs .(37± 7) ;P <0 0 5、ALT活性 (U/L)显著降低 (89± 15 ,6 9± 7;P <0 0 5 ) ,肝硬化肝组织丙二醛含量 (nmol/mg)显著降低 (18 7± 3 2 ,12 0± 2 2 ;P <0 0 5 )、超氧化物歧化酶活性 (U/mg)显著升高 (82 4± 10 8,10 2 9± 76 ;P <0 0 5 )、胶原纤维相对含量 (% )显著降低 (2 2 30± 3 86vs.14 70± 2 0 7;P <0 0 5 ) ,肝硬化大鼠的门静脉压 (cmH2 O)亦显著降低 (14 4± 2 0vs.9 3± 1 5 ;P <0 0 5 )。结论　药理剂量的rhGH能够促进肝硬化大鼠的白蛋白合成、改善肝细胞功能 ,有助于抑制肝组织纤维化、缓解门静脉压力。     

Extended total arch replacement for type B aortic dissection with ascending aneurysm following healed aortic dissection

We describe a case of type B aortic dissection with large ascending aortic aneurysm occurring 12.8 years after aortic root replacement (Cabrol procedure) in a non-Marfan patient with cystic medial necrosis of the aorta. We have successfully performed an extended total aortic arch replacement using a four-branched graft through the “L-indsion” approach (a combination of a left anterior thoracotomy and upper half median sternotomy). Of note, a histological specimen from the aneurysmal ascending aortic wall revealed “healed aortic dissection” with fibrous tissue replacing the media and intima in addition to multiple foci of cystic medial necrosis.     

Hepatic-pericardio-phrenic collateral (natural shunt) in a patient with Budd-Chiari syndrome

Hepatic venous outflow tract obstruction, Budd-Chiari syndrome (BCS), leads to portal hypertension and to the development of collaterals that bypass the obstruction. Described here is a BCS patient with an unusually large transdiaphragmatic collateral between the left hepatic and left innominate veins, which decompressed the oesophageal varices. This has not been reported earlier in the literature.     

Hepatic infarction with portal thrombosis

A case of hepatic infarction with portal thrombosis is reported. A 63-year-old woman with liver cirrhosis and esophageal varices was admitted for treatment of the esophagel varices. Endoscopic variceal ligation (EVL) and endoscopic injection sclerotherapy (EIS) were performed. Two months later, she experienced right hypochondralgia and right flank pain. Serum transaminase levels were suddenly elevated, and computed tomography scans of the liver showed multiple small nodular lesions. Her condition worsened, and she died of hepatic failure. Autopsy revealed splenic and portal vein thrombosis, multiple hepatic infarction, and evidence of chronic pancreatitis. We believe that liver cirrhosis and chronic pancreatitis were the main risk factors for the portal thrombosis, and the treatment for esophageal varices appeared to have triggered the thrombosis. The hepatic infarction was caused by the portal thrombosis.