胰腺微循环通道及其临床意义：光镜和扫描电镜研究

用甲基丙烯酸甲酯微血管铸型扫描电镜观察、血管内墨汁灌注连续切片光镜观察,对20例恒河猴的胰腺微循环通道进行了研究。猴的胰腺微循环通道主要途径为:小叶间动脉→小叶内动脉→入岛血管→胰岛血窦→出岛血管(门脉)→腺泡毛细血管网→小叶内静脉→小叶间静脉。构成胰腺基本单位的胰腺小叶,其血供特点是:由独支小叶内动脉供给血液,相邻小叶内动脉及其分支之间无吻合存在,属终动脉,推测这一特点可能是急性胰腺炎小叶内灶性坏死的形态学基础。     

胰岛的引流系统与胰腺的整体机能

目的研究胰岛引流系统与胰腺外分泌的联系及胰腺门脉循环的意义。方法用微血管树脂／墨汁灌注扫描电镜／光镜观察、ＦＩＴＣ标记红细胞（ＦＩＴＣ－ＲＢＣ）荧光活体显微镜观察，对人、猴、狗、兔、鼠的胰岛血液引流通道进行了系统研究。结果胰岛的血液主要经胰岛的输出血管引流至外分泌腺泡区域，胰岛的引流系统存在对不同腺泡区域产生影响的三种类型。研究者根据胰岛引流系统的特征对其进行了分类及命名：①连续型：行程短、管径细，引流至胰岛周围的腺泡毛细血管区域；②聚合型：管径粗、行程长，引流至远离胰岛的腺泡毛细血管区域；③跨越型：越过小叶间隔引流至另一胰腺小叶的腺泡毛细血管区域，而这一小叶往往没有胰岛存在；胰岛的引流系统构成了胰岛－腺泡的门脉循环。结论胰岛有如此完善的联系外分泌腺泡的引流系统，提示；含有高浓度胰岛内分泌激素的胰岛血液，通过连续、聚合、跨越三种类型的引流系统，到达胰岛周围的腺泡区、远离胰岛的腺泡区以及无胰岛小叶，将对腺泡的机能产生影响，胰腺外分泌的机能有赖于胰岛内分泌激素的支持。结合亚热带地区糖尿病胰腺广泛纤维化病理损伤的特征，研究者推测：胰岛－外分泌微循环的损伤是糖尿病胰腺外分泌病理改变的基础。     

门静脉压升高是胆盐诱发急性胰腺炎微循环障碍的始动环节

有报道,在胆盐诱发的急性胰腺炎早期,胰腺动脉收缩导致了胰腺微循环障碍。本实验的目的就是验证上述发现是否正确。胆胰管内注射牛黄脱氧胆酸钠诱发大鼠和犬胰腺炎;使用活体显微镜观察大鼠胰腺微动脉管径的变化;记录犬胰腺小动脉压的变化;计数机能毛细血管并乘以胰腺湿重校正;用激光多普勒测量胰腺灌流量。我们发现,在诱发胰腺炎后20min内大鼠胰腺微动脉扩张;犬胰腺动脉压从104.5±4.8mmHg降到54.6±5.6mmHg;5min时下腔静脉血的血细胞压积显著低于门静脉血;校正了的胰腺机能毛细血管密度增加。胰腺微循环障碍与门静脉压升高(最多升高9.18±0.78mmHg)同时发生。将门静脉压降低至基础水平可使胰腺灌流量增加约2.4倍。实验显示,在胆盐诱发急性胰腺炎的早期,胰腺动脉发生了扩张而不是收缩;这时门静脉压升高;门静脉压升高大大减小了胰腺血管压差,并导致血浆丢失和局部血液浓缩,导致胰腺微循环障碍。     

胰腺发育学研究进展

1胰腺的解剖学特征 两种不同的组织构成：一是分泌酶类进入消化道的外分泌腺；二是分泌激素进入血液循环的内分泌腺。胰腺的外分泌部为小叶状多分支的复管泡状腺，成群分泌细胞组成腺泡。大部分消化酶类，包括蛋白酶、淀粉酶、脂肪酶和核酸酶，都是以无活性酶原的形式分泌，进入十二指肠后再被激活成为有活性的酶。胰腺的内分泌细胞分布于郎格汉斯胰岛内，胰岛为紧密的球团状组织，嵌于外分泌腺中。     

胰腺腺泡细胞和胰岛β细胞损伤修复及再生的研究进展

胰腺炎可引起胰腺腺泡及胰岛β细胞损伤,修复胰腺内、外分泌功能是胰腺炎治疗研究亟待解决的问题;胰腺损伤修复、胰腺干细胞及内、外分泌细胞的再生和调控再生信号通路(Notch、Hedgehog及Wnt信号)对其意义重大。而胰腺腺泡及胰岛β细胞的损伤修复、再生及调控胰腺内外分泌细胞的去分化、转化和再分化过程是目前研究的热点。     

人胰岛微血管的扫描电镜观察

采用微血管铸型扫描电镜观察法研究了6例成人胰腺内胰岛的微血管构筑，结果发现，成人胰岛由小叶内动脉的分支－胰岛输入血管供应，根据其首先到达胰岛的部位不同将胰岛分为三种类型，即周围型，中央型和混合型；所有胰岛的输出血管－胰岛－腺泡门脉血管均为连续型门脉血管；约1％的胰岛，其输出血管除形成胰岛－腺泡门脉血管外，还可形成胰岛－胰岛门脉血管而到达附近的小胰岛，形成小胰岛毛细血管球。     

卵泡刺激素在大鼠胰腺中的定位及其与促性腺激素释放激素受体共存关系

目的：研究卵泡刺激素在大鼠胰腺中的分布及其与促性腺激素释放激素受体的共存关系。方法：采用免疫组织化学法和邻片双标记方法。结果：大鼠胰腺外分泌部腺泡内的部分腺细胞和胰岛中的部分内分泌细胞呈现FSH免疫阳性反应,阳性产物分布于胞质,胞核阴性。卵泡刺激素与促性腺激素释放激素受体在大鼠胰岛细胞中有重叠分布。结论：大鼠胰腺外分泌部的腺泡细胞和胰岛的细胞能表达卵泡刺激素。卵泡刺激素和促性腺激素释放激素受体共存于大鼠胰岛细胞中。表达卵泡刺激素的胰岛细胞可能受促性腺激素释放激素调节。     

人腮腺微血管构筑

用血管铸型扫描电镜法，观察人腮腺微血管的构筑。从铸型上看，腮腺各小叶的界限分明。小叶的表层为管径粗细一致的毛细血管，它们在腺泡和闰管周围相互吻合成毛细血管网。腺泡和闰管周围毛细血管网起自腺泡微动脉。腺泡微动脉主要起自小叶内动脉，但也可起自小叶间动脉。纹状管周围为毛细血管后微静脉和微静脉相互吻合形成的网状静脉丛。小叶间导管起始部的周围，为一层由毛细血管和毛细血管后微静共同形成的微血管网，随着小叶间导     

大鸨(Otis tarda limaells)胰腺超微结构研究

目的　观察大鸨胰腺超微结构 ,探讨大鸨胰腺功能。　方法　透射电镜观察 3例大鸨胰腺。　结果　大鸨的胰外分泌部为管泡状腺 ,腺小叶由于缺乏叶间结缔组织而界限不如哺乳动物的明显。叶间隙似导管 ,小叶间导管管壁简化以至由胰腺分泌细胞代替。仅在 3个小叶间能见到单个长梭状结缔组织细胞 ,其胞质变细伸展进入两叶间隙中间构成 1条中等密度线。外分泌细胞可分为明暗两种。胰的内分泌细胞呈岛状或单个散布于胰外分泌腺中。胰岛分A和B两种 ;A胰岛仅由A细胞构成。B胰岛主要由B和D两种细胞构成 ,其中B细胞数量多 ;D细胞含量少。　结论　大鸨胰腺具有一些不同于其他动物及适应于飞翔的结构特点     

胃肠激素与胰腺外分泌

胰腺是具有内外分泌双重功能的重要器官。内分泌的胰岛细胞可分为A、B、D、和PP细胞等,分散在外分泌的胰腺腺泡之间。胰腺的内外分泌功能是互相影响,互相调节的。本文主要介绍胃肠激素与胰腺外分泌的关系。 一、胃肠激素对胰腺外分泌功能的调节 胰腺外分泌受神经和激素两方面调节。近年研究发现有些神经调节是通过多肽类神经递质发挥作用。可影响胰腺外分泌的激素     

Morphology of pancreatic microcirculation in the monkey: Light and scanning electron microscopic study

The morphology of the microcirculation of the pancreas in 20 monkeys (Macaca mulatta) was studied by scanning electron microscopy (SEM) of vascular corrosion casts and light microscopy (LM) of China ink-injected/cleared tissues. The principal results were that (1) insulo-acinar portal vessels were found between the endocrine and exocrine parts in the pancreas. The blood flows from the endocrine to the exocrine part. (2) Depending on the different microvascular arrangement, there were two patterns of microcirculation in the islet: in 66% of islets the direction of microcirculation was from cortex to core, and in 44% from core to cortex. (3) Islets could be categorized in three classes on the basis of size: the small islets (40–100 μU in diameter), the intermediate islets (101-240 μU in diameter), and the large islets (241–340 μm in diameter). (4) Insulo-insular portal routes were observed in the pancreas of the monkey. Some intermediate or large islets were connected to an adjacent small islet by one or two, occasionally more, efferent vessels. These small islets received no arterial branch and were entirely supplied by the portal vessels-the efferent vessels of intermediate or large islets. The authors suggest this new pattern to be termed the insulo-insular portal system. (5) A single centrally located intralobular artery as the exclusive vessel supplied each pancreatic lobule of the monkey, there being no anastomosis between the intralobular arteries and any of their branches. This anatomic feature might be the morphological basis of the pancreatic microcirculatory disturbance and microvascular impairment occurring during acute pancreatitis. The functional and clinical significance of pancreatic microcirculation are discussed in the paper. © 1995 WiIey-Liss, Inc.     

THE TERMINAL DISTRIBUTION OF THE HEPATIC ARTERY AND ITS RELATIONSHIP TO THE DEVELOPMENT OF FOCAL LIVER NECROSIS FOLLOWING INTERRUPTION OF THE PORTAL BLOOD SUPPLY

The terminal distribution of the hepatic artery of the human liver was examined by arterial injection of india ink and serial sectioning. The branches of the hepatic artery form capillary networks around the bile duct in the portal tract, from which the capillaries (terminal venous branch) arise and connect with sinusoids at the most peripheral zone of the liver lobules. Evidence of direct anastomosis between the hepatic artery and portal vein inside the portal tract or presence of "innere Pfortaderwurzeln" as well as the intralobular arteriole was not demonstrated.
The authors also studied the hepatic changes caused by interruption of the portal blood supply to the liver lobule. It was demonstrated that the portal tract and its components as well as several layers of liver parenchymal tissue around the portal tract are nourished from blood via the peribiliary capillary plexus and thus remains unaffected by portal obstruction, while other parts of the liver lobule will undergo coagulation necrosis.
Based on the present investigation, the authors believe that the hepatic artery plays the main role in the nourishment of the bile duct while it has little to do with that of the liver lobule, except for the most peripheral layers of the liver lobules adjacent to the portal areas.     

Microcirculation of the rat pancreas, with special reference to the insulo-acinar portal and insulo-venous drainage systems: a further scanning electron microscope study of corrosion casts.

Microcirculation in rat pancreas was studied by scanning electron microscopy of resin vascular casts and by light microscopy of India ink-injected and sectioned tissue samples. In the scanning survey of the casts, islets larger than 30 microns in diameter counted no less than 400 in the adult rat pancreas. They were located either in the exocrine lobules (intralobular islets, counting 210 or more), or in the interlobular tissue spaces and along the secretory ducts (extralobular islets, 190 or more). Every islet received arterial blood via one or more proper arterioles. These afferent vessels first divided in the peripheral zone of the islet consisting of A and D cells and later extended deeper to form a capillary network in the islet core consisting of B cells. Blood originating from this capillary network left the islet via efferent vessels. This microvascular pattern may favor the regulation by A and D cells over the secretory activity of B cells. The intralobular islets gave their efferent vessels to the capillary bed of the exocrine tissue of the lobule, thus forming an insulo-acinar portal system. When the lobule was relatively small in size, superfluent blood was led directly to veins via insulo-venous drainage vessels. The intralobular islets sometimes issued one or more long translobular portal vessels reaching adjacent lobules. The extralobular islets issued either insulovenous vessels draining to interlobular veins, or extralobular insulo-acinar portal vessels supplying adjacent lobules.     

Nitric oxide, heparin and procaine treatment in experimental ceruleine-induced acute pancreatitis in rats.

The aim of the study was to investigate the impact of L-arginine (nitric oxide donor), L-NNA (NO synthase inhibitor), heparin and procaine on the pancreas' microcirculation, serum interleukin 6 (IL-6) level, and microscopic alterations of the pancreatic gland in acute pancreatitis (AP) in rats. AP was induced by 4 i.p. injections of cerulein (15 micrograms/kg/h). Microcirculatory values of the pancreas were measured by means of laser Doppler flowmetry 5 h after the first cerulein injection. Remarkable morphologic changes in the pancreas, including parenchymal necrosis, an elevation of serum IL-6 activity, and significant drop of pancreatic capillary perfusion was observed in rats with NO synthase inhibition. L-arginine improved the pancreatic microcirculation but worsened the microscopic alterations within the pancreas. Heparin had a beneficial effect on the microcirculatory values, serum IL-6 activity, and morphologic changes. Procaine had no effect on the course of AP. Authors conclude that heparin, improving the pancreatic capillary blood perfusion, may be considered as a promising therapeutic agent in acute pancreatitis.     

成年高原藏羊睾丸小叶内微血管分布和形态特征

目的 探讨成年高原藏羊睾丸小叶微血管构筑特征.方法 采用ABS树脂血管铸型技术、扫描电镜观察法、墨汁明胶石蜡切片及常规石蜡切片技术,观察30只成年高原藏羊睾丸小叶微血管的构筑特征.结果 睾丸小叶内由向心或离心动脉发出的管间微动脉及管间毛细血管穿行于相邻生精小管形成的结缔组织间隙内;管间毛细血管相互交通形成管周毛细血管围...     

门静脉压和局部血液表观黏度在急性胰腺炎胰腺微循环障碍中的表达

目的根据Hagen—Poiseuille方程[Q=π（P1-P2）R^4／8／μl],胰腺血管压差（P1-P2）和胰腺血管内血液表观黏度（μ）决定胰腺的血液灌注（pancreatic blood flow,PBF,Q）。因此,本实验研究门静脉压和局部血液表观黏度在急性胰腺炎胰腺微循环障碍中的作用。方法胆胰管内注射牛黄脱氧胆酸钠诱发大鼠和犬急性胰腺炎。记录颈动脉压、门静脉压、胰腺小动脉压和肠系膜上动脉压。用激光多普勒测量大鼠胰腺十二指肠部的血液灌流量。结果在急性胰腺炎的早期,门静脉压（Pvp,P2）增高可达一倍。将门静脉压人为地保持在基础水平,可以诱发急性胰腺炎,10min后大鼠胰腺灌流量增加1．4倍。发生在胰腺内的血浆外渗造成局部血液的血细胞比容显著高于全身其他血管的血液;局部的血液浓缩导致局部的血液表观黏度显著高于他处血液。结论门静脉压升高和局部血液黏度增高是引起急性胰腺炎胰腺微循环障碍的重要机理。     

The microvasculature of the human pancreas and its relation to Langerhans islets and lobules

The 3-D relation between the lobules, terminal blood vessels and Langerhans islets of human pancreas was established by graphic reconstruction from serial histologic sections. The material included three pancreases obtained at autopsy. It was found that the lobule is an assembly of sublobular parenchymal units which have a terminal arteriole at the center. These, being considered to be an elemental structure of microcirculation, were named the "primary lobule" of the pancreas. The concept was also supported by the 3-D analysis of a pancreas "pseudolobulated" due to chronic venous congestion, in which "primary lobules" were clearly demarcated by atrophic zones distributed along the periphery of circulation. Four types of terminal arterioles were discriminated: 1) those terminating at an islet, 2) those having no relation with islet, 3) those with islets dispersed near the ending and 4) those coming directly from an interlobular artery. More than half the endings were found to belong to either Type 2 or 3, which was quite different from the traditional assumption of complete arterio-insular correlation. Consequently, islets could also be classified according to whether or not having an afferent arteriole, namely, into "arterial" and "non-arterial" islets. The "arterial" islets amounted to 75% in the total islet volume, although in islet number, the "non-arterial" ones accounted for as much as 72.5%. Thus, at least in man, functional correlation between islets and exocrine gland is not so tight as claimed by the insulo-acinar axis theory.     

Histological evidence of initiating factors in acute necrotising pancreatitis in man.

In this necropsy review of 37 cases of acute pancreatitis, evidence is presented that there are at least two different initiating mechanisms in acute necrotising pancreatitis in man. Firstly, there is primary duct inflammation, with subsequent inflammation and necrosis of the pancreatic parenchyma surrounding the excretory ducts. Included in this group are cases secondary to alcohol abuse and cholelithiasis. Secondly, there is necrosis confined to the microcirculatory periphery of the pancreatic lobule. These cases are usually secondary to some form of shock (septic or cardiogenic) and are thought to represent ischaemic pancreatitis. These patterns of necrosis are discussed in relation to the pancreatic anatomy and clinical findings.