大鼠下丘脑弓状核年龄性变化的电镜观察

电镜观察大鼠下丘脑弓状核超微结构的年龄变化。结果发现:衰老大鼠弓状核的年龄变化主要发生在弓状核中的暗细胞神经元,出现粗面内质网退化变短,排列失序;高尔基氏器缩小;多聚核蛋白体和神经内分泌物质明显减少。特别引人注目的是在部分暗细胞中出现由双层膜缠绕形成的膜性涡旋体结构。此外,在神经毯出现突触结构异常。突触厚度变薄、间断不连续;神经胶质细胞突起增多,并可进一步形成包绕树突、轴突终末、甚至突触的多层膜环绕的髓鞘样结构。上述研究结果提示,下丘脑弓状核超微结构的年龄性变化是导致神经内分泌系统衰老的主要原因之一。     

先天性心脏病心肌糖原的超微结构观察

电镜下观察30例先天性心脏病心肌糖原的改变。结果表明:先天性心肌细胞内糖原丰富,肌浆游离糖原呈β型,分布在正常心肌相同。4例心肌(占13.3%)观察到线粒体内β型糖原颗粒沉积,16例心肌(占53.3%),出现了髓鞘样结构,其内多含有β型糖原颗粒。线粒体内糖原沉积和贿鞘样结构的出现可能表明心肌慢性局烂性缺氧。     

犬腺垂体远侧部P物质样免疫反应神经纤维的超微结构研究

本室曾在光镜水平上显示,犬腺垂体远侧部P物质样免疫反应多膨体神经纤维与腺细胞关系极为密切。本实验应用包埋前免疫组织化学电镜法,进一步研究了这种神经纤维的超微结构,及其与腺细胞的关系。本文发现P物质样免疫反应多膨体神经纤维与各种腺细胞以及滤泡星形细胞发生直接接触,与促生长激素细胞和促肾上腺皮质激素细胞有典型的突触结构,其中与后者构成的突触较多。大多数突触为不对称型,含有圆形或椭圆形清亮小泡和大致密芯泡。本实验结果表明,犬腺垂体远侧部P物质样免疫反应神经纤维对腺细胞活动有直接调节作用。     

大鼠中枢神经系统衰老的形态学研究—大脑顶叶皮质神经元的超微形态改变

本文对不同年龄雄性Wistar大鼠顶叶皮质神经元的超微结构进行了观察。结果表明随增龄神经元的各种结构发生了明显的形态与数量改变,包括:(1)表面复合器的致密带加长、变宽;(2)高尔基体及粗面内质网分布紊乱,池腔扩张或狭小关闭,线粒体膨胀、固缩或退行性变。脂褐素、各种致密泡、致密体及异常结构增多;(3)核形态较不规则,周边染色质减少,核质致密化,核内包涵物少见。此外,随老化胞突部基质变暗,微管增多,形态变异,壁上有异物附着。     

狗腺垂体远侧部降钙素基因相关肽免疫反应神经纤维的超微结构研究

本实验应用包埋前免疫电镜法,研究了狗腺垂体远侧部降钙素基因相关肽(CGRP)免疫反应神经纤维的超微结构,及其与腺细胞的关系。发现CGRP免疫反应神经纤维与促肾上腺皮质激素细胞和促生长激素细胞构成典型的突触结构,其中与前者之间的突触较多。大多数突触为非对称型,神经终末内含有清亮小泡和大致密芯泡。还观察到许多未被免疫染色的神经终末,它们与促肾上腺皮质激素细胞、促生长激素细胞、催乳激素细胞和促甲状腺激素细胞形成突触。我们还应用包埋后免疫双标记法,发现在狗腺垂体远侧部神经纤维中,P物质样免疫反应物质与CGRP免疫反应物质共存,但它们分布于不同大致密芯泡内。     

老年大鼠下丘脑视上核和弓状核的超微结构变化

观察老年大鼠下丘脑视上核腹侧大细胞神经元和弓状核神经元的超微结构,结果显示:老年大鼠视上核腹侧血管加压素(VP)神经元的胞体较成年鼠大,胞质结构比较致密,内含许多核糖体颗粒,粗面内质网分散成小泡状,神经分泌颗粒增多,溶酶体、线粒体、高尔基氏复合体数量都较多.而弓状核内的暗细胞和亮细胞的核糖体减少,高尔基氏复合体和线粒体都变化,还有少数神经元固缩,细胞质内胞器明显减少,呈现变性现象.结果提示:老年期下丘脑视上核VP神经元机能增强;而弓状核内两种细胞都显示机能减弱的征象.老年时下丘脑各核团神经元的这种不协调性变化,可能是动物衰老的一种重要表现.     

大鼠海马CA_1区锥体神经元在衰老过程中的超微结构变化

本文对不同年龄组雄性ＳＤ大鼠海马ＣＡ_１区锥体神经元的超微结构进行了观实，结果表明随增龄：（１）锥体神经元核周体基质密度有所下降，一些细胞器在数量、形态上也有变化，还见到”空泡变性”现象．（２）锥体神经元核膜出现皱褶，染色质群集或异染色质边集，核内包含物出现，也偶见“空泡变性”现象．（３）胞突中树突发生显著改变．上述结果可能是大鼠老化的一些形态学指征。     

大鼠心肌梗塞后梗塞区胆碱能神经支配的变化

目的：探讨大鼠心肌梗塞区胆碱能神经支配的变化。方法：实验用20只大鼠,以组织化学Karnovsky-Roots法显示胆碱能神经纤维。应用多功能图像分析仪测定梗塞区胆碱能神经纤维密度。结果：大鼠心肌梗塞后4天,梗塞区胆碱能神经纤维密度显著下降;梗塞后14天,梗塞区胆碱能神经纤维完全消失;梗塞后120天,心肌梗塞区的部分区域出现胆碱能神经纤维,结论：大鼠心肌梗塞后14天,梗塞区发生完全的去胆碱能神经支配,120天后部分区域出现胆碱能神经再支配。     

EARLY ULTRASTRUCTURAL CHANGES OF EPITHELIAL CELLS OF THE GLANDULAR STOMACH IN RAT INDUCED BY N-METHYL-N'-NITRO-N-NITROSOGUANIDINE

The early ultrastructural events that occur In the gastric epithelial cells of the glandular stomach of rat from 12 hours to 3 weeks after oral administration of N-methyl-N'-nitro-N-nitrosoguanidine were examined and compared with the X-irradiation effects on mouse gastric mucosa. The mucoid cells of the pyloric mucosa, particularly the surface and pit mucous cells exhibited the greatest ultrastructural alterations among the 6 types of gastric epithelial cells. The earliest changes of the mucoid cells were observed in the nuclei, and were characterized by the sequential development of first nucleolar enlargement, which consisted of the increase of both the fibrillar and granular components, followed by the occurrence of nucleolar segregation, reduction and clumping of the chromatin, and irregularity of the nuclear membrane. Significant degenerative changes of the cytoplasm in the mucoid cells could be observed after these nuclear alterations. Later, giant cell formation in the mucoid cells and mesenchymal cells, and the development of epithelial cells containing two cell specificity were found.
These ultrastructural alterations of the mucoid cells seem to represent the morphologic manifestations of biochemical interaction between N-methyl-N'-nitro-N-nitrosoguanidine and biological materials.     

衰老大鼠禁水时视上核加压素能神经元超微结构变化

电镜观察不同禁水时间衰老大鼠下丘脑视上核加压素能神经元的超微结构变化。结果发现：禁水６、１２ｈ后，视上核加压素能神经元胞体增大，胞质中粗面内质网排列紧密且增多，高尔基复合体成熟面未成熟分泌颗粒及神经分泌颗粒增多；轴突中神经分泌颗粒增多不明显。而禁水２４ｈ后，神经元胞质内的神经分泌颗粒减少，轴突中的神经分泌颗粒聚集成膨大区域。禁水后，神经胶质细胞减少，突起回缩，使相邻的两神经元直接接触，突触结构重建增多。上述研究结果提示，衰老大鼠下丘脑视上核加压素能神经元在禁水时，其功能活动是增强的，胶质细胞突起回缩，有利于神经元之间的突触结构重建。     

超声波辐照后家兔肝脏超微结构的变化

本文作者用诊断剂量的超声波辐照活体家兔肝脏，喂养３ｄ致死后取材，经处理后用电子显微镜观察其超微结构的变化情况。实验结果表明超声波辐照２０ｍｉｎ的家兔肝脏的超檄结构无明显变化，而辐照３０ｍｉｎ及６０ｍｉｎ的家兔肝脏，除细胞质内粗面内质网有程度不同的扩张外，肝组织及肝细胞的其它结构均无明显改变。由于热效应与辐照时间有关，而本实验辐照３０ｍｉｎ及６０ｍｉｎ的家兔肝脏的超微结构的变化是相同的。且本实验所用超声强度小而不致引起机械效应。因此作者认为本实验出现的兔肝细胞粗面内质网扩张的现象不会是热效应和机械效应引起，而只可能是空化效应所致，这说明诊断超声可能在动物组织中引起空化效应。     

急性心功能不全时大脑皮质超微结构的变化

用电子显微镜对10例死于急性左心功能不全的患者大脑额叶、顶叶和颞叶皮质进行了研究.发现毛细血管周围星形胶质细胞的突起水肿,基膜破坏,内皮细胞质空泡化,线粒体变性,溶酶体堆积,毛细血管腔缩窄,紧密连接变性.神经元核内出现膜性包含物.神经细胞及胶质细胞内有纤维性包含物,线粒体变性,胞质空泡化以及脂褐素体沉积.突触的变性表现为突触前末梢肿胀,突触小泡集聚、融合、破坏.     

EFFECT OF MAGNESIUM DEFICIENCY ON ULTRASTRUCTURAL CHANGES IN CORONARY ARTERIES OF SWINE

The effects of magnesium (Mg) deficiency on the coronary arteries of 27 Yorkshire swine were studied by light and electron microscopy. The experimental animals were divided into 4 groups which received the following supplements: Group I, basal ration with adequate Mg (540 mg/kg diet), Group II, basal ration with insufficient Mg (270 mg/kg diet) Group III, 10% milk powder with adequate Mg (540 mg/kg diet), Group IV, 10% milk powder with insufficient Mg (270 mg/kg diet). Serum analysis indicated that dietary low Mg supplementation decreased cholesterol levels and increased phospholipid concentrations significantly. The highest magnitude and incidence of intimal thickening were observed in the coronary arteries of Group IV (p < 0.003). No significant intimal thickening was detected in any of the other groups. Ultra-structural studies revealed a greater frequency of degenerated cells in Group III and IV (p<0.01). Numerous calcifications were observed in only Group IV. These data suggest that moderate Mg deficiency can promote atherosclerosis in combination with some atherogenic diet, and that the presence of smooth muscle cell degeneration is important in order for a magnesium deficiency to exert an effect on the coronary artery of swine.     

大鼠烫伤后早期肝细胞变化的超微结构观察及形态计量分析

用超微结构形态计量方法分析了大鼠30％烫伤后早期肝细胞超微结构的变化规律。烫伤后,肝细胞内精原迅速减少,至6小时,几乎全部消失。烫伤后2小时、6小时。肝细胞内溶酶体的体积密度、数目密度和平均体积均明显增大。线粒体于烫伤后半小时出现基质密度增加、嵴扩张,烫伤后2小时、6小时,线粒体肿胀,其体积密度、平均体积增大。实验结果提示:在严重烧伤后数小时内,肝细胞的超微结构即出现明显的改变。本文对出现这些变化的机制进行了讨论。     

ULTRASTRUCTURAL LOCALIZATION OF PROLACTIN IN THE HUMAN PITUITARY PROLACTINOMAS AND ITS CHANGES BY BROMOCRIPTINE TREATMENT

Fourteen human prolactinomas, four of which received bromocriptine treatment, were studied by immunoelectron microscopy to observe the intracellular localization of prolactin (PRL). In the untreated cases two different patterns of PRL localization were noted. In the first type (Type I) PRL was seen in Golgi saccules, single stacks of rough endoplasmlc retlculum (RER), and a few secretory granules and in the second type (Type II) it was present in the predominant parallel arrays of RER. Type II cells were observed more frequently in the cases with higher serum prolactin levels. In the treated cases with normalized serum prolactin levels, the tumor cells showed accumulation of secretory granules. This finding suggested secretory inhibition. RER and Golgi saccules were inconspicuous in these cells and this might indicate decreased production of PRL. In a case which was resistant to the bromocriptine treatment, most tumor cells were similar in ultrastructural localization of PRL to those cells in the untreated cases and this might suggest the lack of dopamine receptor.     

糖尿病早期大鼠视网膜毛细血管及视细胞超微结构变化规律

目的：探讨大糖尿病视网膜病变（糖网病）早期的视网膜毛细血管及视细胞的病变规律。材料与方法：选择健康成年Wistar大鼠,随机分成正常对照组,糖尿病1月,3月和6月组,一次性腹腔内注射链脲佐菌素STZ）诱导大鼠糖尿病,制备视网膜超薄切片,透镜观察并计算机图像分析。结果：病程1月,周细胞和内皮细胞核异染色质聚集靠边;视杆膜盘间隙略扩大。3月,毛细血管细胞异染色质聚集严重,基底膜增厚;膜盘间隙扩大明显,局灶性断裂,溶解。视杆细胞膜固缩,异染色质浓集,视杆内节线粒体肿胀,甚至空泡变性,病程6月,以上改变更加严重,毛细血管狭窄,变形,甚至闭塞。结论：糖网病早期大鼠视 膜毛细血管病变的同时,变出现视感受器超微结构的改变,随病程的进展病变逐渐加重。     

慢性癫痫模型动物海马内GABA能神经元的超微结构改变

用马桑内酯诱发小鼠性性癫痫模型，借助免疫电镜方法对海马的ＧＡＢＡ能神经元的超微结构进行观察，可见小鼠海马内ＧＡＢＡ免疫反应阳性神经元弥散分布于除锥体细胞层和颗粒细胞层外的各部。慢性癫痫上鼠海马内的ＧＡＢＡ免疫反应性神经元胞体和末梢均呈现程度不同的结构损伤，包括线粒体肿胀，细胞器崩解和神经末梢变性，ＧＡＢＡ样轴突末梢可与免疫反应阴性的树突构成传出性轴－树突触，也可接受免疫反应阴性轴末梢的传入性轴－轴