血吸虫病肝内微血管阻塞部位的研究

本研究采用血管墨汁灌注方法、血管塑料铸型方法,结合扫描电镜和透射电镜。观察了血吸虫病鼠(n=10)和兔(n=10)肝内微血管的变化。发现血吸虫病动物肝内门脉分支中断,肝窦数目减少,肝静脉分支扭曲、变形,肝窦毛细血管化,肝窦内皮细胞损伤,肝窦内有白细胞嵌塞。表明血吸虫病肝不仅有窦前梗阻,肝窦内及窦后亦有梗阻因素存在。     

成年大鼠小肠绒毛微血管构筑的扫描电镜观察

本文应用微血管铸型技术和扫描电镜观察法 ,研究了成年大鼠小肠绒毛微血管的构筑。结果表明 :1大鼠小肠绒毛有一条来自粘膜下层的螺旋形的绒毛微动脉 ;2大鼠小肠绒毛的血液除了由绒毛微静脉汇入粘膜下静脉外 ,还存在一条侧副循环途径 ,即通过绒毛“边缘毛细血管”将血液引流入相邻绒毛的毛细血管网 ;3联系腺丛与绒毛血管丛的微直血管向缺少动脉终末支的绒毛基底部供血 ,主要起到“侧副循环”的作用。     

“肝脏反馈机制”并非门脉高压症高动力循环的发生机制

观察“肝脏反馈机制”在门脉高压症（ＰＨＴ）内脏高动力循环发生过程中的作用，检测了门静脉分支结扎（ＰＢＬ）大鼠和门静脉缩窄肝前型ＰＨＴ（ＰＶＬ）大鼠不同时期的血流动力学变化。结果显示：ＰＢＬ术后７天由于门静脉阻力增加，门静脉压力出现一过性增高，第５，７天出现类似于ＰＶＬ大鼠的短暂的全身高动力循环状态，整个实验过程中，尽管ＰＢＬ大鼠部分肝脏失去了门静脉血供，但未发现象ＰＶＬ大鼠所表现的内脏血管阻力下降     

大鼠肝内型门脉高压症形成中门静脉力学性质的变化

目的观察大鼠肝内型门脉高压症形成中门静脉零应力状态及轴向拉伸时张应力．伸长比关系的动态变化，探讨门静脉生物力学特性的变化在门脉高压症形成中的作用。方法以60％四氯化碳(CCl4)皮下注射法制备肝内型门脉高压症大鼠模型，采用生物力学技术测定CCl4注射第2、4、6、8、10周大鼠门静脉零应力状态张开角和轴向拉伸时张应力，伸长比关系，并同步监测大鼠门静脉压力(PVP)、门静脉流量(PVF)、平均动脉压(MAP)、门静脉阻力(PVR)和内脏血管阻力(SVR)等血液动力学指标的动态变化。结果随着CCl4注射时间的延长，实验组大鼠的血液动力学指标发生了显著的变化。与之相对应．大鼠门静脉张开角及轴向拉伸参数b亦逐渐增大，从注射第10周起与对照组相比具有统计学差异(P＜0．05)。结论门脉高压症大鼠存在高动力循环状态(HCS)。HCS可引起门静脉血管生物力学特性的变化。     

豚鼠肝脏微血管铸型扫描电镜观察

经豚鼠的主动脉灌注低粘度的甲基丙烯酸甲酯,制成肝8庄微血管铸型标本,在双目显微镜下进行解剖,然后镀膜,用扫描电子显微镜观察。在肝脏铸型标本表面,清楚地显示出由肝窦状隙所组成的肝小叶轮廓,在相邻的肝小叶之间,窦状隙的周围部有广泛吻合,放大观察窦状隙的表面,可见有不甚规则而近似圆形的压痕。在肝脏血管铸型的断面标本,可见呈放射状排列的肝窦状隙,它们彼此吻合,并向小叶中心汇集成中央静脉。小叶间Glisson鞘内显示以下结构:小叶间静脉及其与肝窦状隙的吻合支;肝动脉与小叶间静脉伴行,并发出其终末支连于胆管周围丛;胆管周围丛显示为单层毛细血管网,该丛一方面自肝动脉接受其输入血管,另一方面也从该丛发出输出血管,由小叶周围部汇入肝窦状隙,构成胆管周围门脉系统。     

人心室壁微血管构筑的扫描电镜研究

以甲基丙烯酸酯微血管铸型法观察了2例成年男性尸体标本的心室壁微血管构筑,并与实验动物(犬4例、山羊2例、绵羊2例、兔4例、豚鼠4例,大鼠4例)作了比较。结果表明,人和上述实验动物心室壁微血管构筑无明显不同;左、右室壁微血管构筑基本相似。1.左心室肌层毛细血管密度:浅层、中层、深层毛细血管密度相似,均约2,000支/mm~2,肉柱和乳头肌内毛细血管密度较高,约3,000支/mm~2左右。2.微循环单位:心室壁微循环似以肌束区分范围;在肌束内,又可区分出微循环单位。肌束间有与之平行的微动脉和微静脉。由微动脉沿途发出的终末微动脉,垂直进入肌束。在     

兔肝脏及附属管道的应用解剖学研究

目的　对兔肝脏及其附属管道进行应用解剖学研究。 方法　对20只日本大耳兔分别进行活体和离体形态学观察,制作门静脉和肝静脉管道铸型标本观察其分支与走行,测定各肝叶质量及其所占肝脏百分比。 结果　兔肝肝裂明显,依据肝叶形态、肝裂走行和门静脉主干分支形式将兔肝脏分为五叶,分别为尾状叶、左外叶、左中叶、右中叶、右外叶,各肝叶质量分别为(g)：3.93±1.13、15.93±3.50、14.83±3.31、15.08±4.34、12.08±3.55。左中叶和右中叶根部肝组织融合,其余各肝叶相对独立,尾状叶包括相对独立的乳头突和尾状突两部分。各肝叶有相对独立的Glisson系统和肝静脉走行于肝蒂内。 结论　兔肝解剖学特点与多数哺乳类实验动物肝脏解剖相似,同时又具有其自身特点,适合于肝脏外科疾病动物模型的制作。     

肝前型门静脉高压兔门脉系统血管应力的研究

门脉高压症是肝硬化常见的病理生理改变.本研究采用两步门静脉结扎法制备门脉高压症(PHT)兔模型;检测不同时间点门静脉及小肠系膜曲张静脉的直径,不同程度曲张静脉及门静脉主干的血流动力学和应力(压力、剪应力和周向应力)大小.随着小肠系膜曲张静脉直径的增大,PHT兔门脉与小肠系膜静脉压力显著增加,剪应力减小,周向应力增大;两部位间应力(压力、剪应力和周向应力)呈直线正相关.研究表明,门脉高压时门脉系统处于低剪应力与高周向应力状态,这可能是门脉高压症并发症发生的力学基础.     

大鼠肝前性门静脉高压症形成中一氧化氮和内皮素-1水平的动态变化

目的:观察大鼠肝前性门静脉高压症形成中一氧化氮(NO)和内皮素-1(ET-1)水平的动态变化,探讨其在门静脉高压症高动力循环中的作用。方法:以部分门静脉结扎(PVL)法复制肝前性门静脉高压症大鼠模型,分别用硝酸还原酶和放免法检测正常组、假手术(SO)组及PVL组术后不同时点的门静脉血浆NO^-₂/NO^-₃、ET-1水平,并同步监测血流动力学指标的动态变化。结果:PVL术后各时点NO^-₂/NO^-₃水平显著高于而ET-1水平显著低于正常组,同时伴有血流动力学的明显变化。结论:门静脉高压症大鼠存在高动力循环状态(HCS)。NO和ET-1参与HCS的形成和维持。     

一氧化氮合酶抑制剂口服两周治疗对肝硬化大鼠高动力循环状态的影响

目的:观察小剂量一氧化氮合酶(NOS)抑制剂N-硝基-L-精氨酸甲酯(L-NAME)连续2周治疗对肝硬化大鼠高动力循环状态的影响。方法:用60%四氯化碳油性溶液皮下注射SD大鼠制造肝硬化大鼠模型。对肝硬化大鼠,用L-NAME(0.5mg·kg^-1·d^-1)胃管内注入连续治疗2周。用57Co同位素微球技术分别测定L-NAME治疗组、未治疗组及正常对照组的平均动脉压(MAP)、门静脉压(PP)、心输出量(CO)、心脏指数(CI)、内脏血管阻力(SVR)及内脏器官血流量(SBF)。用荧光法测定各组大鼠血清亚硝酸盐含量。结果:未治疗组MAP、SVR显著低于正常对照组,而PP、CO、CI、SBF及亚硝酸盐含量则显著高于正常对照组(P值均小于0.01)。在治疗组,L-NAME显著缓解了CO、CI、SBF及亚硝酸盐浓度的增加和MA、SVR的下降。与未治疗组比较,治疗组血清亚硝酸盐浓度明显减少[(1.471±0.907)μmol/Lvs(4.204±1.253)μmol/L,P<0.01]。结论:内源性NO在肝硬化血流动力学改变中可能起重要作用。小剂量L-NAME连续2周口服治疗可以缓解肝硬化大鼠的高动力循环状态。     

Hemodynamic alterations in cirrhosis and portal hypertension

Portal hypertension (PHT) is associated with hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation. Increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation play a central role in the pathogenesis of PHT. PHT is also characterized by changes in vascular structure, termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the formation of new blood vessels, also occurs with PHT related in particular to the expansion of portosystemic collateral circulation. The complementary processes of vasoreactivity, vascular remodeling, and angiogenesis represent important targets for the treatment of portal hypertension. Systemic and splanchnic vasodilatation can induce hyperdynamic circulation which is related with multi-organ failure such as hepatorenal syndrome and cirrhotic cadiomyopathy.     

汉族与回族人群外周血管阻力及其相关因素的比较

 目的 对宁夏回族自治区银川市汉族与回族人群外周血管阻力的差异及其相关影响因素探讨和分析。方法 采用美国Bioz.com数字化无创血液动力学监护仪，检测了2 795名汉族和1 886名回族人群体循环血管阻力（SVR）、体循环血管阻力指数（SVRI）、收缩压（SBP）、舒张压（DBP）、体质量指数（BMI）、心输出量（CO）、心指数（CI）、心率（HR）、平均动脉压（MAP），同时进行相关因素的分析。结果 1﹚回族16～18岁和30～39岁男性SVR分别显著高于相应年龄的汉族男性（P<0.01，P<0.05）。2）回族16～18岁男性SVRI显著高于相应年龄的汉族男性（P<0.01）。多元线性回归显示：对回、汉两民族之间SVR差异影响的强弱依次为MAP、CI、HR、SBP及DBP；对SVRI影响的贡献大小指标顺序与SVR一致。结论 回族SVR/SVRI高于汉族可能与遗传及生活方式有关。     

On the Mechanisms Responsible for Selection of Hepatic Veins as Target for Thrombosis Following Injection of Endotoxin in Hyperlipemic Rats

The feeding of a butter-rich diet, to sensitize rats for studying the phenomenon of hepatic vein thrombosis, is shown to produce severe liver steatosis leading to a sinusoidal barrage and portal hypertension. The portal pressure in these animals was 210 ± 4 mm of saline, as compared to 113 ± 3 mm in the normal rat. Blood circulation studies using carbon suspensions revealed production of a vascular stasis in the hepatic veins after 60 to 90 minutes, when endotoxin (Salmonella typhosa, 0.3 mg/kg) is introduced into the blood circulation to initiate hepatic vein thrombosis. Similar results were observed after 15 minutes with ellagic acid (1 mg/kg/min). The stasis was found in connection with an additional intrahepatic resistance to blood flow as evidenced by a rise in portal pressure and by a reduction in liver perfusion in relation with development of systemic hypotension. In contrast with this, endotoxin initiated only slight and transient changes in the normal rat. Thrombosis immediately followed production of stasis in the hepatic vein, whether the phenomenon was initiated by endotoxin or ellagic acid. Furthermore, inhibition of the vascular stasis of α-adrenergic blockade (phenoxybenzamine, 3 mg/kg) was accompanied by prevention of hepatic vein thrombosis. It is concluded that stasis in the hepatic veins resulting from a mechanical obstruction of the circulation by steatosis and by an additional reduction in blood flow initiated by endotoxin, is responsible for selection of hepatic veins as targets for thrombosis following injection of endotoxin in hyperlipemic rats.     

Hyperdynamic circulation in portal hypertension: a comparative model of arterio-venous fistula

Complications of portal hypertension remain perplexing physiologic phenomena in the understanding of shunt hemodynamics with multiple theories. Hyperdynamic circulation was also found in sepsis, chronic anemia and arterio-venous (A-V) fistula which relate to an increase in nitric oxide. We hypothesize that portosystemic collaterals may mimic an A-V fistula in which the high-pressure portal blood connects with the lower pressure systemic venous circulation. Although these collaterals decompress the portal circulation, a number of secondary hemodynamic phenomena occur which increase portal blood flow and tend to counteract the portal hypotensive effect of the portosystemic shunt. The consequent increases in cardiac output and portal blood flow perfuse the compromised liver. As portal blood flow increases, collateral flow increases and is nearly totally shunted in the systemic circulation. This shunt may eventually introduce a vicious cycle of hyperdynamic circulation into a compromised host. Ultimately, high-output cardiac failure occurs, leading to cirrhotic cardiomyopathy.     

Hepatocellular prolapse of hepatic portal tracts and subendothelial space of central veins in idiopathic portal hypertension

We report a case of idiopathic portal hypertension (IPH) with unusual liver pathology. The liver showed changes similar to these previously reported in IPH and, in addition, we observed the unusual features of prolapse of hepatocytes into portal tracts and also into the subendothelial space of hepatic veins. Hepatocyte prolapse into hepatic veins has previously been reported only in patients with a history of androgenic steroid therapy and immunosuppressive therapy. We speculate that, in our case, prolapse of hepatocytes could be related to the abnormal intrahepatic blood flow or to intrahepatic vasculopathy.     

Segmentation and reconstruction of hepatic veins and intrahepatic portal vein based on the coronal sectional anatomic dataset

Three-dimensional (3D) reconstruction of intrahepatic vessels is very useful in visualizing the complex anatomy of hepatic veins and intrahepatic portal vein. It also provides a 3D anatomic basis for diagnostic imaging and surgical operation on the liver. In the present study, we built a 3D digitized model of hepatic veins and intrahepatic portal vein based on the coronal sectional anatomic dataset of the liver. The dataset was obtained using the digital freezing milling technique. The pre-reconstructed structures were identified and extracted, and then were segmented by the method of manual intervention. The digitized model of hepatic veins and intrahepatic portal vein was established using 3D medical visualization software. This model facilitated a continuous and dynamic displaying of the hepatic veins and intrahepatic portal vein at different orientations, which demonstrated the complicated relationship of adjacent hepatic veins and intrahepatic portal vein realistically in the 3D space. This study indicated that high-quality 2D images, precise data segmentation, and suitable 3D reconstruction methods ensured the reality and accuracy of the digital visualized model of hepatic veins and intrahepatic portal vein.     

Stroke Volume Variation for Prediction of Fluid Responsiveness in Patients Undergoing Gastrointestinal Surgery

Background: Stroke volume variation (SVV) has been shown to be a reliable predictor of fluid responsiveness. However, the predictive role of SVV measured by FloTrac/Vigileo system in prediction of fluid responsiveness was unproven in patients undergoing ventilation with low tidal volume. Methods: Fifty patients undergoing elective gastrointestinal surgery were randomly divided into two groups: Group C [n₁=20, tidal volume (V_t) = 8 ml/kg, frequency (F) = 12/min] and Group L [n₂=30, V_t= 6 ml/kg, F=16/min]. After anesthesia induction, 6% hydroxyethyl starch130/0.4 solution (7 ml/kg) was intravenously transfused. Besides standard haemodynamic monitoring, SVV, cardiac output, cardiac index (CI), stroke volume (SV), stroke volume index (SVI), systemic vascular resistance (SVR) and systemic vascular resistance index (SVRI) were determined with the FloTrac/Vigileo system before and after fluid loading. Results: After fluid loading, the MAP, CVP, SVI and CI increased significantly, whereas the SVV and SVR decreased markedly in both groups. SVI was significantly correlated to the SVV, CVP but not the HR, MAP and SVR. SVI was significantly correlated to the SVV before fluid loading (Group C: r = 0.909; Group L: r = 0.758) but not the HR, MAP, CVP and SVR before fluid loading. The largest area under the ROC curve (AUC) was found for SVV (Group C, 0.852; Group L, 0.814), and the AUC for other preloading indices in two groups ranged from 0.324 to 0.460. Conclusion: SVV measured by FloTrac/Vigileo system can predict fluid responsiveness in patients undergoing ventilation with low tidal volumes during gastrointestinal surgery.