冷钾稀释血逆灌对心肌缺血再灌注损伤的保护作用

本文对７例进行换瓣手术的风湿性心脏病患者，采用冷钾稀释血冠状静脉窦逆行灌注方法保护心肌，同时利用ＨＰＬＣ检测了手术不同时点心肌能量有关物质的变化，并以此为指标评价顺灌与逆灌的保护效果。结果提示，逆灌较顺灌保护效果好。表现为逆灌时，手术过程中各时点（除停跳立即外，缺血４０分钟，复跳立即，复跳２０分钟）ＰＣｒ检测表观值各时点比顺灌时高；ＡＴＰ检测表观值在复跳２０分钟时逆灌明显高于顺灌，ＡＤＰ和ＮＡＤ检     

纳络酮对缺血再灌注心肌微循环血流量及其超微结构变化的影响

本文观察了纳络酮对犬缺血和再灌注心肌微循环血流量及其超微结构变化的影响。结果表明：心肌缺血再灌注时微循环血流量明显降低（P＜0．01），但再灌注早期（5min），心肌微循环血流量接近正常，缺血40min，再灌注30min，毛细血管周围组织严重水肿，内皮高度肿胀，管腔狭窄，甚至闭塞；纳络酮治疗缺血和再灌注早期，心肌微循环血流量明显增加（P＜0．01）；毛细血管周围组织水肿及管腔狭窄程度明显轻于缺血再灌注组。提示：纳络酮可减轻缺血再灌注心肌的水肿程度，增加微循环血量，推迟“无再流现象”的发生。     

缺血再灌流损伤对肾毛细血管内皮细胞的影响——细胞化 …

应用常规电镜及过氧化氢细胞化学技术，观察了缺血再灌流对鼠肾毛细血管内皮细胞损伤情况后，缺血６０ｍｉｎ可致毛细血管内皮细胞明显肿胀，过氧化氢细胞化学表现为在内皮细胞表面有少量电子致密的沉积缺血６０ｍｉｎ复流１０ｍｉｎ毛细血管内皮细胞表面有大量电子致密物沉积，缺血６０ｍｉｎ复流３０ｍｉｎ及６０ｍｉｎ内皮细胞损伤加重，毛细血管内皮细胞与基底层之间裂开，翻起，甚至剥脱。毛细血管内皮细胞与肾小管上皮细胞之间     

温血逆灌对心肌缺血再灌注损伤的保护作用

本文对１３例风湿性心脏病换瓣手术患者用温血逆灌进行心肌保护，以高效液相色谱检测高能磷酸化合物及其某些降解产物，证明ＡＴＰ和ＰＣｒ含量均呈复跳２０分钟（Ⅳ）＜复跳立即（Ⅲ）＜缺血４０分钟（Ⅱ）＜停跳立即（Ⅰ）的趋势。ＡＤＰ、ＡＭＰ和ＨＹＰＯ具有与上述相反的变化趋势，而ＮＡＤ含量则稍有增高。上述实验结果表明：温血逆灌的心肌中，高能化合物（ＡＴＰ、ＰＣｒ）合成比作者以前用低温高钾稀释血灌注时（正灌＾（１     

无复流现象发生机制及其与心肌挫抑关系的实验探讨

本文在离体鼠心Ｌａｎｇｅｎｄｏｒｆｆ模型上探讨无复流现象的发生机制及其与心肌挫抑的关系。在１５ｍｉｎ低流缺血及１０ｍｉｎ开灌后，心功能降低出现心肌挫抑。形态学检查见心肌水肿，内皮细胞轻度肿胀。体视学检查示开放的毛细血管数明显减少，表明有明确的无复流现象存在。升高灌注液中镁的浓度可显著改善心功能，减轻心肌水肿、内皮肿胀，但无复流现象无改善。结果表明：无复流现象在心肌挫抑发生发展中不起重要作用。心肌水     

微血管内皮大空泡形成对微循环的影响

大鼠肠系膜微血管缺血再灌后内皮细胞出现明显改变,缺血再灌后３０ｍｉｎ～１ｈ细静脉、集合毛细血管内除有白细胞、血小板的粘附以及红细胞聚集、血管内皮水肿外,还发现血管内皮细胞的胞浆形成圆丘形的空泡。空泡从血管内壁内壁突入管腔,空泡直径１０～３０μｍ,多发生在直径２０～７０μｍ的细动脉,静脉内也可出现,但不如动脉多。在同一根血管内可同时出现几个空泡,大的空泡几乎堵塞血管腔。严重者几个空泡出现在同一管腔的周围,造成管腔的堵塞,使血细胞不能顺利通过。结果表明血管内皮大空泡的形成将阻碍血液的流动,加重微循环的障碍和血管周围组织细胞的损伤。     

缺血再灌流损伤对肾毛细血管内皮细胞的影响──细胞化学观察

应用常规电镜及过氧化氢细胞化学技术，观察了缺血再灌流对鼠肾毛细血管内皮细胞的损伤情况。缺血６０ｍｉｎ，可致毛细血管内皮细胞明显肿胀，过氧化氢细胞化学表现为在内皮细胞表面有少量电子致密物沉积。缺血６０ｍｉｎ复流１０ｍｉｎ，毛细血管内皮细胞表面有大量电子致密物沉积。缺血６０ｍｉｎ复流３０ｍｉｎ及６０ｍｉｎ，内皮细胞损伤加重，毛细血管内皮细胞与基底层之间裂开、翻起，甚至剥脱。毛细血管内皮细胞与肾小管上皮细胞之间有电子致密物沉积，甚至肾小管上皮细胞基底部也有致密物沉积。     

地奥心血康对心肌缺血再灌犬血清肾上腺素含量,心脏指数…

杂种犬随机分为地奥心血康治疗组（ＤＫＧ）及生理盐水对照组（ＣＧ）。应用荧光法测定血清去甲肾上腺素（ＮＥ）含量，定时测平均动脉压（ＭＢＰ），心输出量（ＣＯ），计算总外周血管阻力（ＴＰＶＲ），心脏指数（ＣＩ）。结果显示：（１）再灌后的ＭＢＰ在ＤＫＧ与ＣＧ之间无明显差异，Ｐ〉０．０５；（２）再灌２４０ｍｉｎ时，ＤＫＧ中ＣＩ值高于ＣＧ（Ｐ〈０．０１）；ＮＥ值与ＴＰＶＲ值明显低于ＣＧ（Ｐ〈０．０５，Ｐ〈０．     

山莨菪碱对脑血管内皮细胞与自由基的影响

采用电子显微镜观察沙鼠急性缺血再灌注后内皮细胞的变化及山莨菪碱对其的作用，结果发现缺血再灌注组脑血管内皮细胞间隙增宽，紧密连接破坏，采用电子顺磁共振法测定自由基单位重量积分强度为５２９２１．１４２±２．７６５；山莨菪碱组脑血管内皮细胞损伤明显减轻，并且自由基单位重量积分强度为３５５６２．９２６±８．１３７（Ｐ＜０．０５）。说明山莨菪碱能够保护脑血管内皮细胞和具有清除氧自由基作用     

心肌缺血／再灌注对球结膜微循环的影响以及一氧化氮的调节作用

对照观察兔急性心肌缺血／再灌注时球结膜微循环的变化，测定动物血浆中内皮舒张因子／一氧化氮（ＥＤＲＦ／ＮＯ）、血栓素Ｂ２（ＴＸＢ２）、６－酮－前列腺素Ｆ１α（６－Ｋｅｔｏ－ＰＧＦ１α）、超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）的浓度变化，并用光镜和电镜对缺血／再灌注心肌组织作形态学观察。结果发现：（１）兔心肌缺血／再灌注后球结膜微循环异常；表现为Ａ３、Ａ４微动脉血管管径缩小，毛细血管交换距离增大。（２）血浆中ＥＤＲＦ／ＮＯ水平降低；（３）血浆ＴＸＢ２、ＭＤＡ水平升高，ＳＯＤ、６－Ｋｅｔｏ－ＰＧＦ１α下降；（４）光镜下：缺血区心肌组织细胞肿胀变性。电镜下：内皮细胞肿胀，部分毛细血管腔内有红细胞、白细胞附壁阻塞，线粒体肿胀，糖原颗粒减少。结果提示：心肌在较短时间缺血后再灌注（缺血３０ｍｉｎ再灌注３０ｍｉｎ）后就可产生组织损伤，这可能与血管内皮受损，ＥＤＲＦ／ＮＯ合成释放减少，缩血管物质ＴＸＡ２升高，血小板、白细胞粘附、聚集在血管内皮上，氧自由基产生过多等有关。上述因素共同作用导致缺血／再灌注心肌微循环功能障碍进而引起组织形态改变。     

Benign Recurrent Cholestasis: A Light and Electron Microscopic Study with Emphasis on Sinusoidal Cells

A liver biopsy was performed on a patient with benign recurrent cholestasis. Cholestasis was mainly centrolobular with infiltration by sinusoidal macrophages. There was no necrosis. All the classic and specific ultrastructural criteria of cholestasis were observed in hepatocytes under electron microscopy. Perfusion-fixation of the biopsy allowed in addition a good visualization of sinusoids and sinusoidal cells. Numerous macrophages (Kupffer cells) with intense phagocytic activity were present in the lumen; some formed the sinusoidal barrier or were infiltrated in the Disse space. Endothelial cells contained numerous dense bodies and had few fenestrae. Cellular debris of hepatocytic origin which were not phagocytized in the Disse space were extruded in the lumen either through enlarged endothelial pores or by progressive invagination in the endothelial wall followed by outpouching in the sinusoid. In an enlarged Disse space containing amorphous material and collagen fibrils some perisinusoidal cells were transitional cells. These results indicate that pure cholestasis leads not only to hepatocyte injury with intense phagocytic activity but also to some degree of sinusoidal cell damage and extracellular matrix changes.     

Chorioallantoic placenta formation in the rat: II. Angiogenesis and maternal blood circulation in the mesometrial region of the implantation chamber prior to placenta formation

Rat gestation sites were examined on days 7 through 9 of pregnancy by light microscopy and transmission and scanning electron microscopy to determine the extent of vascular modifications in the vicinity of the mesometrial part of the implantation chamber (mesometrial chamber). At a later time, the mesometrial chamber is, in conjunction with the uterine lumen, the site of chorioallntoic placenta formation. On day 7, in the vicinity of the mesometrial chamber, vessels derived from a subepithelial capillary plexus and venules draining the plexus were dilating. By early day 8, this network of thin-walled dilated vessels (sinusoids) was further enlarged and consisted primarily of hypertrophied endothelial cells with indistinct basal laminas. Sinusoids were frequently close to the mesometrial chamber's luminal surface which was devoid of epithelial cells but was lined by decidual cell processes and extracellular matrix. By late day 8, cytoplasmic projections of endothelial cells extended between healthy-appearing decidual cells and out onto the mesometrial chamber's luminal surface, and endothelial cells were sometimes found on the luminal surface indicating that endothelial cells were migrating. The presence of maternal blood cells in the mesometrial chamber lumen suggested that there was continuity between the chamber and blood-vessel lumens. On day 9, the mesometrial chamber was completely lined with hypertrophied endothelial cells, and sinusoid lumens were clearly continuous with the lumen of the mesometrial chamber. Mesometrial sinusoids and possibly the mesometrial chamber lumen were continuous with vessels in the vicinity of the uterine lumen that were fed by mesometrial arterial vessels. Clearing of the mesometrial chamber lumen during perfusion fixation via the maternal vasculature indicated the patency of this luminal space and its confluence with mesometrial arterial vessels and sinusoids. The conceptus occupied an an-timesometrial position in the implantation chamber on days 7 through 9, and it was not in direct contact with uterine tissues in the vicinity of the mesometrial chamber. These observations suggest that angiogenesis, not trophoblast invasion or decidual cell death, plays a major role in the opening of maternal vessels into the mesometrial chamber lumen before the formation of the chorioallantoic placenta.     

Ultrastructural Changes in the Capillary Bed of Human Pituitary Tumors

The fine structure of the capillary bed of the anterior pituitary has been studied in 19 cases of pituitary tumor and 1 autopsy specimen. Tumor specimens were less well vascularized than the autopsy specimen. Endothelial cells within tumor specimens were often observed with swollen portions of cytoplasm, or cytoplasmic blebs, projecting into the capillary lumen. Blebbing, in many cases, nearly obstructed the capillary lumen and was most often associated with endothelial cells that had an electron-lucent cytoplasm, in contrast to endothelial cells that had an electron-dense cytoplasm, even within the same capillary profile. Compared with electron-lucent cells, electron-dense cells contained more endothelial filaments. Also observed were capillaries that had apparently broken apart releasing their contents into the pericapillary space and shrunken remnants of capillaries. A number of abnormal features were observed in the pericapillary spaces—ie, disruption of the parenchymal-pericapillary interface, disorganization of basal laminae, increased amounts of plasma proteins and cellular debris within the space and, ultimately, complete loss of the normal limits and characteristics of the space. Similar, though less pronounced, changes were observed in the autopsy specimen. The hypothesis is advanced that changes observed in the capillary bed are, in large part, a result of tumor growth, which increasingly disrupts tissue organization at the parenchymal-pericapillary interface and, because the tumor mass in the sella turcica can only enlarge upwards, compresses the pituitary stalk and portal veins. The result is ischemia and eventual necrosis. The observations are then in good agreement with recent reports on changes in capillary fine structure associated with ischemia.     

Different preservation of myocardial capillary endothelial cells and cardiomyocytes during and after cardioplegic ischemia (25 degrees C) of canine hearts

Complete resumption of cardiac function after cardioplegic arrest presupposes a well-preserved myocardial ultrastructure during and after ischemia. Therefore, we determined ischemia-induced ultrastructural alterations in the myocardium during and after reversible cardioplegic ischemia using stereological methods. Cardiac arrest was induced with St. Thomas' Hospital- or Custodiol (HTK) solution. Reperfusion with Tyrode's solution followed after reversible cardioplegic ischemia in situ. Samples were taken 1) from beating hearts, 2) from cardioplegically arrested hearts immediately after the end of coronary perfusion, 3) from ischemic hearts incubated in the cardioplegic solution at 25 degrees C, and 4) from reperfused beating hearts after ischemia in situ at 22 degrees C. Cellular swelling was determined as the barrier thickness of capillary endothelium and as the sum of cardiomyocyte volume fractions of free sarcoplasm and mitochondria. In St. Thomas'-arrested hearts, intraischemic volume increase was significantly more pronounced in endothelial cells than in cardiomyocytes. Reperfusion at the intraischemic practical limit of resuscitability (ATP levels of 4 micromol/gww) significantly reduced intraischemic swelling of cardiomyocytes, but not of capillary endothelial cells. Mitochondrial damage was more pronounced in capillary endothelial cells during ischemia and after reperfusion. Thus, after reversible cardioplegic arrest, structural recovery of cardiomyocytes is better than that of capillary endothelial cells. An incomplete structural protection of capillary endothelial cells may predominantly contribute to postischemic dysfunction in the reperfused heart.     

Analysis of intrapulmonary vessels and epithelial-endothelial interactions in the human developing lung

The establishment of a sufficiently wide and functional blood-gas interface is of critical importance in lung development, but development of the intrapulmonary vascular system including alveolar capillary vessels still remains unclear. In this study, we first characterized the structural development of the vascular system in accordance with that of airways in human fetal lungs at the pseudoglandular phase (8, 13, and 16 weeks gestation) by examining the immunohistochemical distribution of CD34 and alpha-smooth muscle actin (SMA). Using double immunohistochemistry and 3-dimensional reconstruction techniques, endothelial cells in the developing lung could be classified into two different types according to the characteristics of their adjacent cells (presence or absence of SMA-positive cells) and their distribution (proximal or distal lung parenchyme). Endothelial cells without SMA-positive cells developed into a capillary network surrounding the budding components of distal airways during the mid-pseudoglandular phase before communicating with proximal vessels. We then examined the immunoreactivity of thrombomodulin and von Willebrand factor (vWF) in endothelial cells. Endothelial cells of the capillary network were mainly positive for vWF during the early gestational stages, but altered their phenotypes to those of mature lungs (vWF negative and thrombomodulin positive) during the terminal sac phase. We subsequently determined the immunohistochemical distribution of vascular endothelial growth factor (VEGF). Epithelial cells of the most distal airways were intensely positive for VEGF. These results suggest that VEGF present in airway epithelial cells is involved in the maturation as well as proliferation of capillary endothelial cells. Epithelial-endothelial interactions during lung development are considered very important in the establishment of the functional blood-gas interface.     

视神经损伤后视神经及其内毛细血管的早期超微结构的变化

目的观察视神经损伤后视神经和神经内毛细血管的超微结构变化,探讨视神经损伤的机制。方法建立家兔视神经损伤的动物模型,利用透射电子显微镜观察视神经及神经内毛细血管超微结构的变化。结果视神经损伤0.5h后,轴突部分肿胀,髓鞘疏松,微管、微丝排列出现紊乱,线粒体肿胀,毛细血管内皮细胞中的吞饮小泡和微绒毛明显减少;损伤6h后,线粒体出现髓样变和空泡样变性,血管内皮细胞肿胀,管腔变窄;损伤12h后,轴突空泡样变性,髓鞘脱失,毛细血管周围间隙增宽;损伤48h后,轴质密度增加,部分髓鞘板层完全分离,微管、微丝及线粒体发生颗粒性溶解,内皮细胞中的线粒体出现广泛变性;损伤96h时,轴索崩解呈空泡状变性,髓鞘更广泛崩解,毛细血管扩张破裂,红细胞外溢。结论视神经损伤早期轴突肿胀、空泡样变性,线粒体水肿变性,微管、微丝数量减少;视神经内毛细血管扩张,通透性增加。     

Changes in the microvasculature of ischemic and infarcted myocardium.

The fine structure of the small vessels in experimental myocardial infarcts of 10- to 360-minute duration was studied in 32 dogs and compared with the appearance of the small vessels in the corresponding normal myocardium. Following 10 to 60 minutes of coronary artery occlusion, increasing numbers of endothelial cells showed a marked swelling which was consistent with the presence of an intracellular edema and frequently resulted in various degrees of obstruction of the vessel lumen. After 120 minutes of ischemia, not all endothelial cells were obviously swollen, but all showed signs of degeneration, including changes in organelles similar to those in surrounding muscle cells. A progressive intensification of degenerative changes, particularly with respect to the continuity of the endothelial lining and the integrity of the membrane systems of individual endothelial cells, was observed at 3, 4, 5, and 6 hours after coronary artery ligation, and cell debris could be seen in the lumina of most small vessels.     

人球结膜微淋巴管电镜观察

目的 :通过白内障病人球结膜的观察 ,获取组织间的细胞裂解产物等进入淋巴管过程的系列图像 ,进一步认识微淋巴管的功能。方法 :6例白内障病人 ,在手术时取球结膜 ,常规制作标本 ,用H 70 0 0、JEM 12 3电镜观察。结果 :淋巴前间隙是连接组织通道和初始淋巴管的特殊腔隙 ,其外形不规则 ,腔壁没有内皮细胞被覆、仅有纤维束样结构 ,局部有多个洞隙。初始淋巴管管腔由不连续到比较完整的内皮细胞包绕。部分区段管腔闭锁 ,局部内皮呈直角向外突出。可见终端开放。内皮细胞相互间为一般接连 ,外无基底膜 ,直接与胶原纤维接触。壁有多个孔隙。小淋巴管的内皮细胞较薄 ,相邻细胞重叠 ,小器官不发达。内皮细胞外没有基底膜。外周胶原纤维比较松散。附近有组织肥大细胞。小淋巴管和初始淋巴管腔内有退变红细胞 ,弥散的血红蛋白 ,多数散在无界膜和有界膜 ,形状不等、较模糊的结构。首次在球结膜观察到由立方内皮细胞构成的细静脉 ,它是循环血中的淋巴细胞进入球结膜的路径 ,参与局部的免疫反应。结论 :淋巴前间隙确实存在 ,它是组织通道和初始淋巴管连通的特殊腔隙。初始淋巴管、小淋巴管没有基底膜 ,壁有退变裂解碎片洞隙。获得了淋巴管排除组织间大分子物质的直接图像。首次在球结膜观察到由立方内皮细胞构成的细