神经生长因子对大鼠心肌梗塞后胆碱能神经的保护作用

目的　观察神经生长因子(NGF)对大鼠心肌梗塞后胆碱能神经的影响,探讨NGF对心肌梗塞的可 能治疗作用。方法　SD大鼠20只制心梗模型,其中10只心梗后给予NGF为实验组,2天后取材,同时取正常心肌 作对照。以Karnovsky Roots法,显示胆碱能神经纤维,应用多功能真彩色病理图像分析系统分析胆碱能神经纤维 密度。结果　心梗左心室心肌梗塞区及梗塞周围区存活心肌中胆碱能神经纤维密度比正常组明显降低(P<0. 01);实验组应用NGF后胆碱能神经纤维密度较心梗组升高。结论　神经生长因子能增加大鼠心肌梗塞后胆碱能 神经纤维的密度,可能对心梗有治疗作用。     

大鼠心肌梗死后AChE阳性神经纤维再支配的观察

目的：观察大鼠心肌梗死后，梗死灶边缘区乙酰胆碱酯酶（AChE）阳性神经纤维密度的变化，探讨AChE阳性神经纤维的再支配过程。方法：实验用大鼠，结扎左冠状动脉前降支制备急性心肌梗死（AMI）模型，应用Kamovsky--Roots法和电镜组化技术，显示左心室梗死周围区1、2、12周AChE阳性神经纤维的密度变化。结果：①AMI后1、2周左心室梗死边缘区的AChE阳性神经纤维密度降低（P〈0．05），②12周后梗死边缘区的AChE阳性神经纤维密度升高，接近对照组。③电镜下见AChE阳性反应物以散在颗粒形式出现于肌间神经纤维走行处。结论：大鼠急性心肌梗死后12周，梗死周围区的存活心肌出现了神经再支配。     

中西药结合促进心梗后大鼠胆碱能神经的恢复

目的：观察葛根素与神经生长因子联合应用对大鼠心肌梗死后去胆碱能神经支配的影响，以证实二者联合应用对心梗后大鼠胆碱能神经功能恢复的作用。方法：实验用SD大鼠32只，分为正常组、心肌梗死组、神经生长因子组及联合用药组。术后2d取材，以Karnovsky-Roots法，显示胆碱能神经纤维，应用多功能真彩色病理图像分析系统分析胆碱能神经纤维密度。结果：心肌梗死组存活心肌中胆碱能神经纤维密度最低，联合用药组胆碱能神经纤维密度最高。结论：葛根素与神经生长因子联合应用能够明显减缓大鼠心肌梗死后的去胆碱能神经支配，促进神经功能的恢复。     

生长激素释放肽对心衰大鼠植物神经重构的影响

本研究观察了生长激素释放肽(GHRP)的应用对心衰动物胆碱能神经和肾上腺素能神经支配的影响。Wistar大鼠50只,随机分为:假手术组10只;GHRP组30只;模型组10只。心衰模型成功后4周,Karnovsky-Roots法及免疫组织化学方法分别显示心肌胆碱能神经纤维及肾上腺素能免疫阳性纤维,应用多功能真彩色病理图像分析系统分析两种神经纤维密度。结果显示,模型组大鼠心肌中胆碱能神经纤维和肾上腺素能神经纤维密度明显低于假手术组(P<0.01);GHRP组大鼠心肌中两种神经纤维密度较模型组明显增高(P<0.01),但略低于假手术组神经纤维密度(P<0.05)。上述研究表明GHRP可延缓大鼠心衰后的去神经支配,改善神经重构。     

哺乳动物垂体后叶比较化学神经解剖学Ⅱ.NT和CCK免疫阳性神经纤维在？…

本文报道了神经紧张素和胆囊收缩素免疫阳性神经纤维不仅存在于大鼠垂体后叶，也存在于猴和狗的垂体后叶。神经紧张素免疫阳性神经纤维在３种动物垂体后叶均为少量稀疏分布，狗和大鼠稍密集，猴最少；猴和狗垂体柄及其邻近的神经叶相对较多，大鼠垂体后叶形成弥散的阳性纤维网，局部可见岛状增密的纤维簇。胆囊收缩素阳性纤维以大鼠垂体后叶密度为最大，狗次之，猴最少；大鼠垂体后叶的中等密度的胆囊收缩素阳性纤维网，吻侧部多于尾     

葛根素对大鼠心肌梗死后梗死部位肾上腺素能神经纤维的影响

目的观察葛根素对大鼠心肌梗死后梗死部位。肾上腺素能神经纤维分布的影响，以求证实葛根索的神经保护作用。方法Wister大鼠120只，分为假手术组、心肌梗死模型组和葛根素组。分别于术后6h、2、4、7、14时取材，应用免疫组织化学方法，显示肾上腺素能神经纤维，应用多功能真彩色病理图像分析系统分析。肾上腺素能神经纤维的密度。结果心肌梗死模型组大鼠在术后6h、2、4、7、14时，梗死区肾上腺素能神经纤维密度均比假手术组明显降低（P〈0．01）。葛根素组大鼠在术后7、14d时，梗死区。肾上腺素能神经纤维密度较心肌梗死模型组明显增多（P〈0．01）；与假手术组相比无显著差异（P〉0．05）。结论葛根素能干预大鼠心肌梗死后的肾上腺素能神经纤维分布减少，具有神经保护作用。     

脑血管的肽能神经支配

<正> 传统认为,脑血液循环的调节有4种机制参与,即化学调节、代谢调节、机械调节及神经调节。其中,神经调节机制的发现经历了较长一段时间,十九世纪后叶,Willis发现大脑前、后动脉有神经纤维分布,不久,Benedikt及Aronsone报告这些脑血管上的神经纤维可能来自颈交感丛。1967年,Nielsen和Owman~(23)发现脑血管的各个部分都有密集的含去甲肾上腺素神经纤维分布,至此脑血管神经支配的概念才真正得以建立。     

大鼠心瓣膜神经支配

本文通过对32只大鼠心瓣膜进行胆碱酯酶组织化学法、乙醛酸诱发荧光法及P物质免疫组化方法的观察,获得心瓣膜胆碱能、肾上腺素能及肽能(SP)神经支配全貌。P物质免疫反应阳性神经纤维在房室瓣自瓣膜基部向下及自腱索向上进入瓣膜;在动脉瓣自附着缘进入瓣膜。该纤维的性质及走向提示SP免疫反应阳性神经纤维可能是感受血流动力学变化的传入神经。     

人和大鼠输精管平滑肌和神经的形态学研究

本实验用组织化学、电镜和生化测定方法研究了人和大鼠输精管的平滑肌和神经分布。结果表明;大鼠输精管的神经密度明显高于人,轴索数/100个肌细胞断面,大鼠是118,人是315肌-神经间隔,大鼠是25nm左右,人是100nm左右;肌细胞外间隙(％),大鼠是12.9,人是35.8;肾上腺素能神经支配占优势,乙醛酸诱发荧光法显示大鼠输精管肌层内有致密的肾上腺素能神经纤维,ACh阳性反应神经较少,主要分布于固有层,人输精管中上述两种神经均较少;每克湿组织中NE含量(ng)大鼠约为人的10倍左右(大鼠:2369.35±820.27,人:294.66±83.90);电镜观察,SGV型神经终末支多见。     

糖尿病大鼠神经形态和山梨醇含量的变化及黄腐酸钠的作用

本研究观察糖尿病大鼠神经元梨醇、神经形态变化及探讨黄腐酸钠对其防治效果。成模6个月后观察（1）目前剂量的黄腐酸钠治疗6个月未能影响糖尿病动物的高血糖。（2）糖尿病组神经山梨醇明显增高；黄腐酸钠治疗组神经山梨醇明显低于糖尿病组，接近对照组水平。（3）糖尿病组有髓神经纤维密度明显低于对照组，电镜下可见神经纤维结构改变；黄腐酸钠治疗组有髓神经纤维密度明显高于糖尿病组，但尚低于对照组，神经纤维超微结构改变黄腐酸钠组较糖尿病组明显减轻。以上提示糖尿病大鼠在病程6个月时出现早期糖尿病神经病变，黄腐酸钠可一定程度地抑制实验性糖尿病周围神经病变的进展。     

骨髓间充质干细胞膜微粒促进大鼠心肌梗死后血管新生

目的:观察骨髓间充质干细胞膜微粒(MSC-MPs)对大鼠心肌梗死后血管新生以及心功能的影响。方法:提取Sprague-Dawley大鼠MSCs并培养,在低氧低营养条件下培养72 h,以诱导细胞凋亡释放MSC-MPs。将培养上清液超速离心获取MSC-MPs,透射电镜下观察其大小及形态,并用流式细胞术分析其表型。建立SD大鼠心肌梗死模型,心肌梗死边缘区注射膜微粒及对照试剂。超声心动图检测心功能,Masson染色检测心梗面积,免疫组织化学染色技术检测梗死边缘区血管α-平滑肌肌动蛋白和von Willebrand因子以确定血管新生情况,real-time PCR检测心梗组织中血管内皮生长因子(VEGF)表达变化。结果:MSCs凋亡后可以释放膜微粒,MSC-MPs来自MSCs,直径为100~1 000 nm。心肌梗死大鼠心肌内注射MSC-MPs后,第7天和第28天时心功能明显改善,第28 d时心梗面积比对照组减小,新生血管密度明显增加,第7天时心梗组织VEGF的表达增加。结论:MSC-MPs可以促进大鼠心肌梗死后的血管新生,改善心功能。     

同种异体骨髓间充质干细胞移植在心肌梗死后心室重建中的作用

BACKGROUND:Myocardial infarction leads to ischemic changes in the myocardium, triggering the emergence of ventricular remodeling, which is an important cause of death. Myocardial infarction is a common disease in the middle-aged and elderly population, but autologous bone marrow mesenchymal stem cells from these patients exhibit a weak ability of proliferation and differentiation. Therefore, a positive attempt of allogeneic stem cell transplantation is required in order to obtain better therapeutic outcomes. OBJECTIVE:To explore the effect of allogeneic bone marrow mesenchymal stem cells on ventricular remodeling after myocardial infarction.   METHODS:Bone marrow mesenchymal stem cells from 10 neonatal rats and 10 adult rats were isolated, cultured and identified. Another 40 rats were randomly assigned into four groups (n=10/group): model group, neonatal rat cell transplantation group, adult rat cell transplantation group, or sham group. Animal models of myocardial infarction were made in rats in the all groups except for the sham group in which the rats were given sham operation. Rats in the two cell transplantation groups were given the corresponding cell transplantation. Four weeks postoperatively, heart function of rats was detected in each group, and cardiac tissues were taken to detect changes in collagen formation and blood vessel density in the infarct area. RESULTS AND CONCLUSION:Four weeks after surgery, rats in the model group showed significant changes in cardiac function indexes as compared with the other groups (P < 0.05), while compared with the model group, these cardiac function indexes improved in both two cell transplantation groups, but there was no significant difference between the two cell transplantation groups (P > 0.05). Meanwhile, compared with the model group, significantly decreased collagen formation and increased blood vessel density were found in both two cell transplantation groups (P < 0.05). Additionally, the vascular density of the infarct area was highest in the sham group (P < 0.05). Experimental results show that both neonatal and adult rat bone marrow mesenchymal stem cell transplantation can improve cardiac function of rats, reduce the formation of collagen in the infarct area and delay ventricular remodeling after myocardial infarction.     

大鼠自体移植脾组织GAP-43+神经再生的实验研究

目的 研究大鼠自体脾组织移植术后移植脾组织GAP-43^ 神经纤维再生及分布规律。方法 健康Wistar大鼠105只，随机分为自体脾组织移植组和对照组，于术后7、15、30、60、90、120、180d取移植脾组织标本，应用免疫组化方法显示GAP-43^ 神经纤维，并用图像分析系统，对不同时相点免疫组化GAP-43^ 染色区域进行图像定量分析。结果 自体脾组织移植术后30d，移植脾组织周围大网膜内可见GAP-43^ 神经纤维，并向移植脾组织内伸展；自体脾组织移植术后60～120d，移植脾组织内再生神经纤维逐渐增多；术后180d，移植脾组织中GAP-43^ 神经纤维分布及密度接近正常。结论GAP-43^ 神经纤维于脾移植术后60d开始出现，术后180dGAP-43^ 神经纤维接近正常脾。     

Diffusion tensor imaging of left ventricular remodeling in response to myocardial infarction in the mouse

The cardiac muscle architecture lies at the basis of the mechanical and electrical properties of the heart, and dynamic alterations in fiber structure are known to be of prime importance in healing and remodeling after myocardial infarction. In this study, left ventricular remodeling was characterized using diffusion tensor imaging (DTI) in a mouse model of myocardial infarction. Myocardial infarction was induced in mice by permanent ligation of the left anterior descending coronary artery. Serial ex vivo DTI measurements were performed 7, 14, 28, and 60 days after ligation. Apparent diffusion coefficient, fractional anisotropy, the three eigenvalues of the diffusion tensor, and the myofiber disarray served as readout parameters. After myocardial infarction, the mouse hearts displayed extreme wall thinning in the infarcted area, which covered large parts of the apex and extended into the free wall up to the equator. Average heart mass increased by 70% 7-60 days after infarction. Histological analysis showed that the infarct at 7 days consisted of unstructured tissue with residual necrosis and infiltration of macrophages and myofibroblasts. At 14 days after infarction, the necrotic tissue had disappeared and collagen fibers were starting to appear. From 28 to 60 days, the infarct had fully developed into a mature scar. DTI parameters showed dynamic changes as a function of time after infarction. The apparent diffusion coefficient in the infarcted region was lower than in remote regions and increased as a function of time after infarction. The fractional anisotropy was higher in the infarcted region and was maximum at 28 days, which was attributed to the development of structured collagen fibers. Myofiber disarray, which was analyzed by considering the alignment of fibers in neighboring voxels, was significantly higher in infarcted regions. DTI provides a valuable non-destructive tool for characterizing structural remodeling in diseased myocardium.     

大鼠急性心肌梗死模型制作方法的改良

目的:为大鼠急性心肌梗死模型制作提供更快、更稳定的方法。方法:所有大鼠按气管插管方法-开胸扩开第3肋间隙方法随机分为:灌胃针-开睑器组(传统组)、灌胃针-缝合线开睑器组、自制插管-开睑器组、自制插管-缝合线开睑器组(改良组),麻醉后分别用相应方法行气管插管和开胸,暴露术野,结扎冠状动脉前降支,记录每组大鼠气管插管时间、气管插管次数、手术时间、术后呼吸道哮鸣音发生率、肺损伤程度和死亡率。术后第2天和第4天随机取各组大鼠5只,行心电图、左心室插管和心肌染色检测模型心功能及心肌梗死面积。结果:使用自制插管的两组插管时间和次数与使用灌胃针的两组差别无统计学意义,但术后呼吸道哮鸣音发生率及死亡率明显低于使用灌胃针两组;使用缝合线开睑器的两组手术时间、术中肺损伤程度及术后死亡率明显低于使用开睑器的两组;各组间心功能及心肌梗死面积差异无统计学意义,改良组组内心功能及梗死面积差异性较小。结论:改良后大鼠急性心肌梗死模型制作方法简单、成活率较高、模型质量较高,值得推广。     

基底膜基质胶携带人脂肪组织来源间充质干细胞移植改善心肌梗死大鼠心脏功能

目的:应用基底膜基质胶(matrigel)携带人脂肪组织来源间充质干细胞(ADMSCs)在大鼠的心肌梗死部位注射,观察其对细胞存活的影响及改善心梗模型大鼠心脏功能的能力。方法:分离、培养、扩增人ADM-SCs,左冠状动脉前降支结扎法建立大鼠急性心肌梗死模型。将大鼠急性心肌梗死模型随机分为4组,对照组(PBS组)、matrigel组、PBS+ADMSCs组、matrigel+ADMSCs组,对移植4周后细胞的存活及心梗局部新生血管的密度进行测量,并利用心脏超声检测大鼠心脏功能。结果:与其它各组相比,matrigel+ADMSCs组的细胞4周存活细胞数量以及心肌梗死区域新生血管密度均显著提高,心脏超声结果也表明该组大鼠的心脏功能改善最为显著。结论:基底膜基质胶能够提高人脂肪组织来源间充质干细胞在大鼠心肌梗死部位的存活,有助于提高心肌梗死部位微血管生成并改善心肌梗死大鼠的心脏功能。     

Intravenously Injected Mesenchymal Stem Cells Home to Infarcted Myocardium Without Altering Cardiac Function

Background： Systemic delivery of mesenchymal stem cells （MSCs） to the infarcted myocardium is an attractive noninvasive strategy, but therapeutic effect of this strategy remain highly controversial. Methods： Myocardial infarction was induced in female Sprague-Dawley rats by transient ligation of the left anterior descending coronary artery for 60 min. Either 2.5 × 106 DiI-labeled MSCs or equivalent saline was injected into the tail vein at 24 h after infarction. Results： Three days later, MSCs localized predominantly in the infarct region of heart rather than in the remote region. MSCs were also observed in spleen, lung and liver. At 4 weeks after infarction, echocardiographic parameters, including ejection fraction, fractional shortening, left ventricular end-diastolic and end-systolic diameters, were not significantly different between MSCs and saline groups. Hemodynamic examination showed that ± dp/dtmax were similar between MSCs and saline-treated animals. Histological evaluation revealed that infarct size and vessel density were not significantly changed by MSCs infusion. Conclusion： Intravenously injected MSCs can home to infarcted myocardium, but plays a limited role in cardiac repair following myocardial infarction.