膈淋巴管三维构型和淋巴吸收机制的研究

采用自行合成的新型铸型剂PAES－3，用扫描电镜淋巴管铸型技术对5例人胎膈淋巴管的三维构型进行研究。人胎隔淋巴管分布较密集，多形成淋巴管网。隔淋巴管网主要由集合淋巴管、淋巴吻合管和毛细淋巴管组成。在膈肌性部，有两层淋巴管网，即浆膜下淋巴管网和深淋巴管网，两者由丰富的淋巴吻合管相沟通；在膈中心腱部，仅一层淋巴管网，淋巴吻合管与集合淋巴告密集相连，呈密网状。膈中心腱部淋巴管网较膈肌性部密集。在膈淋巴管网中，毛细淋巴管常延续为呈扁平状膨大的淋巴陷窝。在集合淋巴管和淋巴吻合管的表面，有许多切迹和缩窄。经透射电镜证实，这些切迹和缩窄即是淋巴管瓣膜所在部位。通过本实验，对腹膜腔淋巴转归径路有了较明确的认识。     

人体下肢淋巴管器官外的结合

淋巴道形态学,尤其是器官外淋巴管连接形式,对了解淋巴侧枝循环的发生,疾病传播途径都有一定意义.本文材料为150具下肢,用各种颜料分别注入浅深淋巴管、血管中,在双筒放大镜、立体显微镜下进行剖解观察.起始于皮肤、皮下的二级淋巴管皆与小动脉伴行,彼此间在动脉分为皮支及筋膜支处汇合后,多数进入与动脉主干或皮下静脉干伴行的淋巴集合管;在腘窝及腹股沟部直接进入淋巴结.皮肤,皮下的淋巴管与相邻的肌、腱、骨膜,关节囊的淋巴管间,筋膜淋巴管与肌、腱、骨膜,关节囊的淋巴管     

腹膜孔与腹水转归机理的研究

应用扫描电镜、透射电镜和ODO冷冻断裂技术,对16例人体样本的腹膜孔进行研究;并为证实腹膜孔作为腹水吸收的主要通路,作了动物实验。结果表明:人体腹膜孔位于膈腹膜立方形间皮细胞之间,由相邻细胞的胞质突起围成。构成腹膜孔的立方形间皮细胞和腹膜孔无基底膜。在立方形间皮细胞的胞质内有成束的微丝。在腹膜下小管内,有由间皮细胞的胞质突起和结缔组织形成的纤维网格,并构成腹膜孔的底和淋巴陷窝的顶。在动物实验中,腹水小鼠的腹膜孔数量增多。口径变大;注入小鼠腹膜腔内的红细胞和碳颗粒被腹膜孔所吸收。本实验结果提示,立方形间皮细胞胞质内的微丝、腹膜下小管内的间皮细胞胞质突起和纤维网格,对腹膜孔的吸收起调节作用,腹膜孔是腹水转归的主要通道。     

腹膜透析液对小鼠腹膜间皮超微结构的影响

目的应用美国Ｂａｘｔｅｒ腹膜透析液和国产乳酸盐、醋酸盐腹膜透析液进行持续性不卧床腹膜透析动物实验,以观察和比较不同类型透析液对正常小鼠腹膜间皮的损伤作用。方法分别将３种透析液注入各组小鼠腹膜腔内,在透析第１０天、第２１天和停药后第１０天取膈腹膜,作电镜观察。结果注入透析液后第１０天,乳酸盐组和醋酸盐组腹膜间皮发生病理变化并随着透析时间延长而进行性加重,出现微绒毛脱落和粘连、间皮细胞皱缩和纤维蛋白性粘连。Ｂａｘｔｅｒ组间皮细胞的病理变化表现轻微。注入透析液后第２１天,乳酸盐组和醋酸盐组的腹膜淋巴孔直径分别为（６．９６±２．４６）和（６．９８±２．１６）μｍ,明显大于对照组（１．４７±０．８８）μｍ（Ｐ＜０．０１）;淋巴孔的分布密度与对照组比较差异亦有显著性（Ｐ＜０．０１）,而Ｂａｘｔｅｒ组的淋巴孔直径及分布密度均无明显变化。停止注射透析液后第１０天,Ｂａｘｔｅｒ组间皮细胞恢复正常;乳酸盐组和醋酸盐组均有不同程度恢复,但淋巴孔仍呈病理改变。结论乳酸盐和醋酸盐腹膜透析液易引起腹膜间皮细胞纤维化,导致硬化性腹膜炎的发生。     

腹膜淋巴孔研究的新进展

腹膜淋巴孔是腹膜下毛细淋巴管在腹膜间皮细胞间的开口。通过淋巴孔、腹膜腔与淋巴管系直接相通,它具有主动吸收功能,是腹膜腔内物质转归的最主要部位。淋巴孔与肝硬化腹水的转归、连续不卧床腹膜透析的失超滤、肿瘤细胞的转移和扩散等密切相关。淋巴孔还具有调控和免疫功能。ＮＯ对淋巴孔调控作用是目前研究的热点,它通过激活鸟苷酸环化酶途径,增加细胞内ｃＧＭＰ,降低Ｃａ＾２＋水平,使淋巴孔产生强烈的舒张,淋巴孔开放数目增多、孔径增大,淋巴引流作用增强。而中药通过提高内源性ＮＯ水平,也能对腹膜淋巴孔进行调控,以促腹水转归。     

大鼠膈淋巴液形成机制的研究

目的　探讨大鼠膈淋巴液形成的机制。方法　大鼠腹膜腔内注射兔血和示踪剂后 ,应用透射电镜观察膈腹膜及膈毛细淋巴管的变化。结果　膈腹膜间皮和膈毛细淋巴管均发生了明显的变化。结论　影响膈淋巴液形成的主要因素为膈腹膜吸收孔和呈开放性连接的毛细淋巴管 ,囊泡系统在膈淋巴液形成和物质转运中也起一定作用 ;管腔内表面突起具有释放作用 ,管腔外表面突起具有吸收作用     

腹膜超微结构与腹膜透析(综述)

近几十年来,由于腹膜透析的广泛应用,国外许多学者对与腹膜透析(contiunous ambulatory peritoneal dialysis, CAPD)有关的腹膜间皮超微结构作了研究.作者在前人研究的基础上,对人和动物腹膜的间皮细胞、微血管、毛细淋巴管和腹膜孔进行了较系统研究.现就腹膜超微结构及其在     

大鼠直肠肛梳区的淋巴管形态结构

目的:观察大鼠直肠肛梳区淋巴管的分布和形态结构特点,探讨大分子物质淋巴道转运的形态学基础. 方法:应用半薄切片和超薄切片技术行光镜及电镜观察大鼠直肠肛梳区的淋巴管结构. 结果:大鼠肛梳区的毛细淋巴管见于真皮乳头层,网状层、皮下组织、肌间可见到比较丰富毛细淋巴管和淋巴管. 毛细淋巴管内皮细胞中含有大量的囊泡;内皮细胞连接有重叠、嵌插和端端连接三种类型,有的处于开放状态. 结论:肛梳区的淋巴管分布与皮肤的相似,大分子物质转运以囊泡系统和内皮细胞连接开放两种途径.     

膈腹膜吸收间皮扫描电镜图像处理系统定量研究

应用扫描电镜、电镜与计算机联机数字图像处理系统对小鼠膈腹膜进行观察、图像复原、图像数据化处理和统计分析，并根据腹膜间皮形态和功能提出吸收间皮概念。同时，还以测定吸收间皮分布面积揭示腹膜对物质的转归作用。实验结果表明，全膈腹膜吸收间皮以板块状正偏态分布，最大板块面积１１５３μｍ＾３，最小６６μｍ＾２，其中左膈和右膈腹膜吸收间皮均以正态分布。全膈、左膈和右膈腹膜吸收间皮板块平均面积分别为４３２．６μｍ     

胸膜淋巴孔的研究进展

淋巴孔是毛细淋巴管在间皮面的开口 ,故又称间皮孔(ｍｅｓｏｔｈｅｌｉａｌｓｔｏｍａｔａ)。淋巴孔通过其下的淋巴引流单位 (ｌｙｍ ｐｈａｔｉｃｄｒａｉｎａｇｅｕｎｉｔ,ＬＤＵ)与起始毛细淋巴管 (即淋巴陷窝 ,ｌｙｍ ｐｈａｔｉｃｌａｃｕｎａｅ)相连 ,从而使胸膜腔与脉管系直接沟通 ,成为引流胸腔内物质进入淋巴管的直接通路[1～ 3] 。胸膜淋巴孔与胸水形成和转归机制 ,感染性微生物和肿瘤细胞胸腔内转移等都有密切的关系 ,为此引起了许多学者的高度关注。 1975年Ｗａｎｇ[4 ] 首次在胸膜上发现了淋巴孔的存在 ,随后一些学者又对胸膜…     

膈淋巴管发育及其与腹腔直接通连的过程

（1）目的：探讨膈淋巴管的发育及淋巴管小孔与腹腔直接通车的过程。（2）方法：应用组织化学，氢氧化钾腐蚀，扫描电镜及透射电镜观察等方法，对174只Wistar大鼠膈淋巴管的发育过程进行了观察。（3）结果：胚胎第16天，膈淋巴管首先出现在膈胸腔面的两侧部，此阶段内皮细胞含有大量的粗面内质网，线粒体，高尔基体和少理的吞饮泡。胚胎第18天，淋巴管内开始出现瓣膜，生后第42天，集合淋巴管长有平滑肌。肌胚第19天，膈的腹腔面开始出现淋巴管，随着年龄增长，胸腔面的淋巴管发出枝芽互相连接形成多角形淋巴管网，腹腔面的淋巴管形成梯形网。生后第0天，膈淋巴管小孔开始开孔于腹腔，此阶段以后，淋巴管小孔急剧增加直至生后第70天。（4）结论：Wistar大鼠膈淋巴管出现于胚胎期；出生后，膈淋巴管开始具有运送腹腔液体的功能。     

腹腔巨噬细胞产生一氧化氮对腹膜透析失超滤的作用

目的 研究腹腔巨噬细胞产生的一氧化氮（ＮＯ）对腹膜淋巴孔的作用,探讨腹膜淋巴孔的淋巴重吸收对长期腹膜透析失超滤的影响。方法 应用腹透液建立腹宁的小鼠模型,用全自动酶标仪动态测定怛,用扫描电镜观察不同时间点腹膜间皮超微病理变化,使用计算机与扫描电镜联机的图象处理系统,测定不同腹膜透析时间点腹膜淋巴孔的变化。结果 腹腹膜管析时程延长,透析组有大量巨噬细胞从腹膜淋巴孔游出,在腹膜表面形成许多乳斑。巨噬细     

REGULATING EFFECTS OF VASCULAR ENDOTHELIAL GROWTH FACTOR AND ANGⅡ ON FROG'S PERICARDIAL STOMATA, MESOTHELIUM AND ANGIOGENESIS

Objective. To observe the regulating effects of vascular endothelial growth factor (VEGF) and angiotensinⅡ (ANG II) on the frog's pericardium, lymphatic stomata and angiogenesis so as to reveal their effects and mechanism on the mesothelial permeability, lymphatic stoma regulation and myocardial hypertrophy. Methods. VEGF and ANGⅡ were injected into the frog's peritoneal cavity so as to examine the changes of the pericardial stromata by using transmission electron microscopy, scanning electron microscopy and computerized imaging analysis. Results. Scattered distributed pericardial stomata were found on the parietal pericardium of the frog with a few sinusoid mesothelial cells, whose blood supply was directly from the cardiac chambers flowing into the trabecular spaces of the myocardium (because there are no blood vessels in the myocardium of the frog). The average diameters of the pericardial stomata in VEGF and ANGⅡ groups were 1.50 μ m and 1.79 μ m respectively, which were much larger than those in the control group (0.72 μ m, P< 0.01); the average distribution densities of the stomata were 8.25/0.1 mm2 and 12.80/0.1 mm2 in VEGF and ANGⅡ groups, which were also much higher than those in the control group (3.57/0.1 mm2, P< 0.01); the sinusoid areas in VEGF and ANGⅡ groups were 2442.95 μ m2/0.1 mm2 and 2121.79 μ m2/0.1 mm2, which were larger than that in the control group (995.08 μ m2 /0.1 mm2 , P< 0.01); no angiogenesis was found in the frogs of the experimental groups. Conclusions. VEGF and ANGⅡ could strongly regulate the pericardial stomata by increasing their numbers and openings with larger diameters and higher distribution density. They could also increase the sinusoid areas with the result of the higher permeability of the pericardium, which clearly indicated that VEGF and ANGⅡ could speed up the material transfer of the pericardial cavity and play an important role in preventing myocardial interstitial edema. Yet there was no strong evidence to show the angiogenesis in the myocardium.     

REGULATING EFFECTS OF VASCULAR ENDOTHELIALGROWTH FACTOR AND ANG 11 ON FROG‘S PERICARDIAL STOMATA, MESOTHELIUM AND ANGIOGENESIS

OBJECTIVE: To observe the regulating effects of vascular endothelial growth factor (VEGF) and angiotensin II (ANG II) on the frog's pericardium, lymphatic stomata and angiogenesis so as to reveal their effects and mechanism on the mesothelial permeability, lymphatic stoma regulation and myocardial hypertrophy. METHODS: VEGF and ANG II were injected into the frog's peritoneal cavity so as to examine the changes of the pericardial stromata by using transmission electron microscopy, scanning electron microscopy and computerized imaging analysis. RESULTS: Scattered distributed pericardial stomata were found on the parietal pericardium of the frog with a few sinusoid mesothelial cells, whose blood supply was directly from the cardiac chambers flowing into the trabecular spaces of the myocardium (because there are no blood vessels in the myocardium of the frog). The average diameters of the pericardial stomata in VEGF and ANG II groups were 1. 50 microm and 1.79 microm respectively, which were much larger than those in the control group (0.72 microm, P < 0.01); the average distribution densities of the stomata were 8. 25/0.1 mm2 and 12.80/0.1 mm2 in VEGF and ANG II groups, which were also much higher than those in the control group (3.57/0.1 mm2, P < 0.01); the sinusoid areas in VEGF and ANG II groups were 2442.95 microm2/0.1 mm2 and 2121.79 microm2/0.1 mm2, which were larger than that in the control group (995.08 microm2/0.1 mm2 , P < 0.01); no angiogenesis was found in the frogs of the experimental groups. CONCLUSIONS: VEGF and ANG II could strongly regulate the pericardial stomata by increasing their numbers and openings with larger diameters and higher distribution density. They could also increase the sinusoid areas with the result of the higher permeability of the pericardium, which clearly indicated that VEGF and ANG II could speed up the material transfer of the pericardial cavity and play an important role in preventing myocardial interstitial edema. Yet there was no strong evidence to show the angiogenesis in the myocardium.     

血管内皮细胞生长因子和血管紧张素Ⅱ对蛙心包间皮,淋巴？…

目的 观察血管内皮细胞生长因子（ＶＥＧＦ）和血管紧张素Ⅱ（ＡＮＧⅡ）对蛙心包间皮、淋巴孔和心肌生血管的作用,探讨ＶＥＧＦ和ＡＮＧⅡ对心包间皮的通透性、淋 的调控作用和心肌肥厚的影响。方法 应用ＶＥＧＦ和ＡＮＧⅡ蛙腹膜腔注扫描电镜和光镜观察,计算机图象处理。结果 正常蛙心包壁层有一些散在２的心包淋巴孔秒量血窦是皮。蛙心肌无血管,其血供仅由心腔内血液直接进入心肌小梁间隙。ＶＥＧＦ组和ＡＮＧⅡ组的心包淋     

Morphological changes of the peritoneum in peritoneal dialysis patients

Background Long-term peritoneal dialysis (PD) requires that the peritoneal membrane remain effective for dialysis. Research directed toward human peritoneal morphology and structure is limited.The present study was performed to investigate morphological changes of the human peritoneal membrane during PD and to elucidate the possible mechanisms of its functional deterioration.Methods A total of 32 peritoneal biopsies were performed in normal subjects (n = 10), uremic nondialysis patients (n = 12) at the time of catheter insertion, and PD patients (n = 10) at the time of catheter removal or reinsertion or at the time of renal transplantation. Peritoneal morphology was examined by light microscopy, scanning electron microscopy, and transmission electron microscopy.Results The peritoneal membrane in normal subjects consisted of a monolayer of mesothelial cells on a basement membrane and a layer of connective tissue containing cells, blood vessels, and lymphatic vessels. MesotheUal cells were polygonal, often elongated, and had numerous microvUli on their luminal surface. There were lots of oval or roundish pinocytotic vesicles in the cytoplasm of themesothelial cells. The peritoneal morphology of uremic nondialysis patients was similar to that of normal subjects. However, significant abnormalities of the peritoneal membrane were observed in PD patients, and the changes were found to be progressive. Microvilli were the first site of damage which involved microvilli shortening, a gradual reduction in their number, and, eventually, the total disappearance of microvilli. Mesothelial cells then detached from the basement membrane,disappearing completely in some cases. In the end, the peritoneal membrane consisted only of submesothelial connective tissue without any cells.Conclusions PD can modify peritoneal morphology and structure. The morphological change is progressive and may be one of the important causes of peritoneal failure. Peritoneal biopsies can provide lots of valuable information about the effects of PD. Studying the relationship between peritoneal structure and its function proved very useful for understanding the physiopathology of the peritoneum during PD.