天津市公安民警颈动脉内中膜厚度与代谢综合征的关系

目的 分析天津市警察人群颈动脉内中膜厚度与代谢综合征 （MS） 的关系, 探讨颈动脉内中膜增厚的危险因素。方法 在体检警察人群中筛选出 50 例 MS 患者为 MS 组及 50 例健康体检者为对照组, 对其进行问卷调查（家族史、 既往史、 现病史、 生活习惯、 职业紧张因素等）; 检测相关血液指标（空腹血糖、 三酰甘油、 总胆固醇、 高密度脂蛋白胆固醇、 低密度脂蛋白胆固醇、 同型半胱氨酸等）; 应用彩超测量其颈动脉内中膜厚度, 计算颈动脉内中膜增厚比率; 比较 2 组的相关指标, 用 Logistic 回归模型分析颈动脉内中膜增厚的影响因素。结果 MS 组的双侧颈总动脉、 颈内动脉、 颈外动脉内中膜厚度及内中膜增厚比率均高于对照组; 高血压家族史、 应激事件、 现吸烟、 糖尿病家族史、 高脂饮食、 高同型半胱氨酸血症是颈动脉内中膜增厚的危险因素, 饮用奶制品是其保护因素。结论 颈动脉内中膜增厚的原因具多样性, 健康的生活方式及采取临床干预措施减缓颈动脉内中膜增厚, 有利于控制动脉粥样硬化。     

彩色多普勒超声对代谢综合征与颈动脉粥样硬化相关性的研究

目的利用彩色多普勒超声研究代谢综合征（MS）与颈动脉内中膜厚度变化的相关性。方法将45例MS患者作为MS组,41例随机选择的正常糖耐量者作为对照组,应用日本东芝SSA-350A彩色超声诊断仪观察各组颈动脉内中膜厚度及斑块状况,以所测量最大内中膜厚度及斑块发生率为观察指标。结果MS组双侧颈动脉内中膜增厚及斑块形成率显著高于对照组（P〈0．01）。结论彩色多普勒超声能确定MS与颈动脉粥样硬化的密切相关性,为MS患者心脑血管病变的早期预防和治疗提供客观依据。     

长期高脂饲料喂养对大鼠主动脉结构的影响

目的观察长期高脂饲料喂养对大鼠主动脉结构的影响。方法SD大鼠14只,分为对照组和实验组。实验组给予高脂饲料12wk后,取主动脉常规制备标本,用光镜、透射电镜和扫描电镜观察。结果实验组主动脉内膜增厚,内皮细胞损伤脱落,有单核细胞黏附;弹力膜断裂,平滑肌细胞增生。透射电镜下内皮细胞的胞膜破溃,呈虫蚀样改变。内皮细胞的线粒体肿胀、空泡变,嵴溶解、断裂、消失;内质网扩张。内皮细胞间隙增大,细胞连接失去正常形态。并可见黏附于内皮表面的单核细胞伸出伪足潜入内皮间隙、内皮下层。有的基底膜随内皮细胞完全脱落。平滑肌细胞粗面内质网和核糖体增多。扫描电镜下内皮细胞肿胀,细胞表面呈大小不等的虫蚀状或火山口状,细胞间出现深大的缝隙。结论长期高脂饲料喂养大鼠可引起主动脉的内皮和弹力膜损伤,单核细胞黏附并侵入内皮和内皮下层,内皮下层和平滑肌增生。     

代谢综合征与颈动脉内中膜厚度的相关性探讨

目的 探讨代谢综合征(MS)与颈动脉内中膜厚度(IMT)的关系.方法 将368例住院患者分为MS组、高危MS组和非MS组,应用血管彩色超声检测颈动脉内中膜厚度(IMT),对各组进行相关性分析.结果 MS组、高危MS组和非MS组的颈动脉粥样硬化斑块形成率分别为54.75%、33.21%和12.04%;3组颈动脉中重度狭窄率分别为48.65%、40.54%和10.81%;3组颈动脉闭塞率分别为70.59%、29.41%和0%,MS组和高危MS组较非MS的颈动脉内中膜厚度(IMT)呈显著增加(P＜0.05).MS的患病分布即具备诊断条件的个数与颈动脉内中膜厚度(IMT)相关.结论 代谢综合征及高危代谢综合征人群是颈动脉粥样硬化斑块形成的危险群体,颈动脉超声检测可作为脑血管病一级预防的预测手段.     

螺旋藻激酶对动脉粥样硬化模型大鼠血管内皮功能的影响

目的:研究螺旋藻激酶(SPK)对动脉粥样硬化模型大鼠血管内皮功能的影响。方法:将60只大鼠随机分为正常对照组(蒸馏水)、模型组(蒸馏水)、阳性对照组(辛伐他汀,0.005 g/kg)和SPK低、中、高剂量组(80、160、320 U/kg)。除正常对照组外,其余各组大鼠均复制动脉粥样硬化模型;同时,各组大鼠ig相应药物,每天1次,连续给药12周。测定大鼠血清中总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)的含量;苏木精-伊红染色观察大鼠胸主动脉血管内膜的形态改变。结果:与正常对照组比较,模型组大鼠血清中TC、TG、LDL-C、IL-6和TNF-α含量增加(P<0.01),HDL-C含量降低(P<0.01);血管内皮细胞脱落,内膜增生、向管腔内突起,平滑肌细胞增殖且排列紊乱,中膜弹力纤维崩解断裂。与模型组比较,各给药组大鼠血清中TC、TG、LDL-C、IL-6和TNF-α含量下降(P<0.05或P<0.01),阳性对照组和SPK中、高剂量组大鼠血清中HDL-C含量增加(P<0.05);给药组大鼠血管内皮细胞形态较模型组明显改善,其中SPK中、高剂量组大鼠血管内皮细胞各层结构完整、内膜基本光滑,SPK中剂量组大鼠血管中膜平滑肌细胞排列稍紊乱,与正常对照组比较无明显变化。结论:SPK有明显的降脂和抗炎作用,可保护血管内皮功能;其作用机制可能与降低血清中TC、TG、LDL-C、IL-6、TNF-α含量和升高血清中HDL-C含量有关。     

补阳还五汤对动脉粥样硬化大鼠主动脉超微结构的影响

目的观察补阳还五汤(BYHWT)对动脉粥样硬化(AS)大鼠主动脉超微结构的影响。方法用高脂饲料加维生素D3的方法建立AS大鼠模型。将40只AS大鼠随机分为模型组(0.9%Na Cl 10 m L·kg^-1)、对照组(辛伐他汀0.6mg·kg^-1)和低、高剂量实验组(BYHWT 10,20 g·kg^-1),每组10只;另取20只正常大鼠随机分为空白组(0.9%Na Cl 10 m L·kg^-1)和预防组(BYHWT 10g·kg^-1,造模的同时给药),每组10只。造模成功后,干预28 d。在透射电镜下观察大鼠主动脉内皮细胞、平滑肌细胞的超微结构。结果高剂量实验组、对照组、预防组的病变均明显轻于模型组,内皮细胞大多形态正常,较完整,内弹力膜较均匀、平直,平滑肌细胞排列整齐。模型组内皮及内皮下层可见到大量泡沫样细胞,有纤维粥样斑块形成,内弹力膜厚薄不一,甚至缺失,平滑肌细胞胶原纤维增生,管壁结构紊乱,胞浆含较多脂质。结论补阳还五汤可改善或纠正AS大鼠模型血管内皮细胞及平滑肌细胞异常的超微结构。     

普伐他汀对鼠动脉粥样硬化及炎症因子的影响

目的 研究普伐他汀对鼠动脉粥样硬化形成过程及炎症因子的影响.方法 取40只大鼠制作动脉粥样硬化模型,随机分为正常饮食组（A）、对照组（B）、普伐他汀（C,10mg＆#183;kg-1＆#183;d-1）、普伐他汀（D,20mg＆#183;kg-1＆#183;d-1）各10只.B、C、D组定期腹腔注射维生素D破坏内皮细胞,喂养3个月,抽血检测hs-CRP,IL-6,并解剖大鼠制作病理切片,最后处死所有大鼠.结果 B组病理切片显示内膜明显增厚,管壁弥漫性隆起,内皮下含大量泡沫细胞,中膜平滑肌细胞增生.而A组内膜光滑,内皮下未见泡沫细胞,中膜平滑肌排列整齐有序,未见增生改变,C、D组内膜增生情况较B组轻,较A组重,且C组较D组增生明显.炎症因子hs-CRP,IL-6在B、C、D、A中的检测水平依次下降,B组较A组、B组较C组、B组较D组、C组较D组差异均有统计学意义（P＜0.05）.结论 普伐他汀有降低炎症因子,抑制动脉粥样硬化形成的作用.     

实验性糖尿病大鼠主动脉的早期改变

观察了链脲佐菌素 ( streptozotocin STZ)致实验性糖尿病大鼠主动脉早期超微结构及转化生长因子β1 ( TGFβ1 )的改变 ,并探讨了糖尿病动脉粥样硬化 ( AS)的发病机制。结果显示 ,STZ糖尿病大鼠出现持续高血糖、高血脂 ,主动脉早期出现内膜增厚 ,内皮下间隙变宽 ,内弹力板破坏 ,内膜和中膜浅层平滑肌细胞增生及部分向内膜迁移。免疫组化显示糖尿病大鼠主动脉内 TGF-β1 表达明显高于正常大鼠。     

兔、豚鼠动脉粥样硬化模型的建立

目的：建立兔、豚鼠动脉粥样硬化模型,探讨模型形成机制并进行比较.方法：用高脂饲料喂养法建立兔、豚鼠动脉粥样硬化模型.高脂饲料喂养,检测血清甘油三脂（TG）、总胆固醇（TC）、高密度脂蛋白（HDL）和低密度脂蛋白胆固醇（LDL）、一氧化氮（NO）、肿瘤坏死因子（TNF-α）的含量,动脉病理组织学检测.结果：兔模型组TC、TG、LDL、NO、TNF-α升高,HDL降低,与正常组比较有显著性差异（P＜0.05,0.01）.豚鼠TC、TG、LDL、HDL、NO、TNF-α升高,与正常组比较有显著性差异（P＜0.05,0.01）.两种动物模型组组动脉病理检测均不同程度出现动脉内膜明显增厚,纤维隆起明显,内皮细胞肿胀、变性、部分缺失,内弹力膜断裂、模糊,中膜增厚伴平滑肌细胞增生,胞体变大,排列紊乱,内膜及中膜均可见巨噬细胞.结论：兔动脉粥样硬化诱导时间比豚鼠短,成模率比豚鼠高,病变更显著.     

曲张大隐静脉管壁病理改变与临床病期的关系

目的研究曲张大隐静脉管壁病理改变与临床分期的关系,为临床治疗提供依据。方法收集不同临床分期的曲张大隐静脉上、中、下三段管壁标本,制作切片分别在光镜和电镜下进行观察。结果光镜下上、中、下三段均出现管壁厚薄不一,内膜增厚不均匀,中膜平滑肌排列紊乱,弹力纤维分离变性、胶原纤维不规则增生、平滑肌增生、萎缩等改变。电镜下上、中、下三段平滑肌细胞胞浆内粗面内质网、核糖体和线粒体等细胞器较多,肌丝较少,中、下段平滑肌有细胞器形态的改变。结论大隐静脉曲张时静脉管壁光镜下全程的病理改变相似,而电镜下血管壁上、中、下三段平滑肌细胞器的改变不同,但其变化与临床分期无关。     

Effect of manidipine on balloon catheter-induced arterial smooth muscle cell proliferation in spontaneously diabetic GK rats.

The inhibitory effect of manidipine, a long acting calcium channel blocker, on vascular smooth muscle cell proliferation was investigated in spontaneously diabetic GK rats with balloon catheter-induced denudation of the carotid artery. Treatment with manidipine at doses of 4.6 and 15.1 mg/kg/day inhibited thickening of the neo-intima in the balloon catheter-injured artery without any effect on blood pressure and lowered the ratio of intima to wall areas and wall to total vascular areas in a dose-dependent fashion. These results suggest that manidipine inhibits an abnormal proliferation of the intima in the carotid artery of spontaneously diabetic rats.     

Fas配体基因对大鼠颈动脉损伤后血管中层平滑肌细胞密度的影响

目的:探讨腺病毒载体介导Fas配体(FasL)基因导入对大鼠颈动脉损伤后血管中层平滑肌细胞密度的影响。方法:实验分治疗组(Ad-FasL组)和正常对照组两组(Ad-βgal组),每组动物均为6只。利用重组腺病毒载体分别将Ad-FasL、Ad-βgal导入大鼠颈动脉球囊损伤的内膜,3、14d后观察其对血管中层平滑肌细胞密度的影响。结果:与正常对照组相比较,通过腺病毒载体介导导入FasL基因的被球囊损伤的大鼠颈动脉,3d后损伤血管中层平滑肌细胞密度降低,14d后血管中层平滑肌细胞密度恢复到正常水平。结论:FasL可抑制血管中层平滑肌细胞密度,从而抑制球囊损伤后的内膜增生。     

Oral exposure to cadmium and mercury alone and in combination causes damage to the lung tissue of Sprague-Dawley rats

Environmental presence and human exposure to heavy metals in air and cigarette smoke has led to a worldwide increase in respiratory disease. The effects of oral exposure to heavy metals in liver and kidney structure and function have been widely investigated and the respiratory system as a target is often overlooked. The aim of the study was to investigate the possible structural changes in the lung tissue of Sprague-Dawley rats after oral exposure for 28 days to cadmium (Cd) and mercury (Hg), alone and in combination at 1000 times the World Health Organization’s limit for each metal in drinking water. Following exposure, the general morphology of the bronchiole and lungs as well as collagen and elastin distribution was evaluated using histological techniques and transmission electron microscopy. In the lungs, structural changes to the alveoli included collapsed alveolar spaces, presence of inflammatory cells and thickening of the alveolar walls. In addition, exposure to Cd and Hg caused degeneration of the alveolar structures resulting in confluent alveoli. Changes in bronchiole morphology included an increase in smooth muscle mass with luminal epithelium degeneration, detachment and aggregation. Prominent bronchiole-associated lymphoid tissue was present in the group exposed to Cd and Hg. Ultrastructural examination confirmed the presence of fibrosis where in the Cd exposed group, collagen fibrils arrangement was dense, while in the Hg exposed group, additional prominent elastin was present. This study identified the lungs as target of heavy metals toxicity following oral exposure resulting in cellular damage, inflammation and fibrosis and increased risk of respiratory disease where Hg showed the greatest fibrotic effect, which was further, aggravated in combination with Cd.     

兔颈总动脉破裂粥样硬化斑块模型的建立

目的建立负压吸引激发兔颈总动脉粥样硬化斑块破裂,建立破裂斑块模型。方法将30只健康雄性新西兰白兔随机分为3组,分别为对照组（n=10）、高脂饲养组（n=10）和球囊损伤＋高脂饲养组（n=10）。饲养8周后,彩色多普勒超声测量颈总动脉内径、内-中膜厚度（IMT）及颈动脉血流速度等,评估动脉IMT与动脉粥样硬化程度的关系。采用＂腔外负压＂法诱导斑块破裂并处死动物,观察诱发斑块破裂成功率,在肉眼及光镜下观察颈动脉内膜形态特征。结果球囊损伤＋高脂饲养组、高脂饲养组的颈总动脉血流速度显著快于对照组,IMT显著厚于对照组,颈总动脉内径显著短于对照组;球囊损伤＋高脂饲养组的颈总动脉内径显著短于高脂饲养组,IMT显著厚于高脂饲养组,颈总动脉血流速度显著快于高脂饲养组（P〈0.05）。球囊损伤＋高脂饲养组可见平滑肌细胞增生,脂质、炎症细胞、泡沫细胞浸润,符合不稳定性斑块特征,有8例诱发斑块破裂,1例死亡;高脂饲养组可见内膜下脂质沉积,炎症细胞浸润,但内皮细胞完整,内弹力板排列整齐,1例诱发斑块破裂,无动物死亡;对照组内皮细胞完整,中层平滑肌细胞排列整齐,无一例诱发斑块破裂,无动物死亡。结论本实验建立动脉粥样硬化斑块破裂模型成功率高,动物死亡率低,实验操作简便易行,为冠心病的生理、病理及药物学效应方面研究提供了可靠的实验平台。     

Modulation of smooth muscle cell proliferation and migration: role of smooth muscle cell heterogeneity

Proliferation and migration of smooth muscle cells (SMCs) from the media towards the intima are key events in atherosclerosis and restenosis. During these processes, SMC undergo phenotypic modulations leading to SMC dedifferentiation. The identification and characterization of factors controlling these phenotypic changes are crucial in order to prevent the formation of intimal thickening. One of the questions which presently remains open, is to know whether any SMCs of the media are capable of accumulating into the intima or whether only a predisposed medial SMC subpopulation is involved in this process. The latter hypothesis implies that arterial SMCs are phenotypically heterogenous. In this chapter, we will describe the distinct SMC phenotypes identified in arteries of various species, including humans. Their role in the formation of intimal thickening will be discussed.     

糖尿病大鼠冠状动脉平滑肌细胞中大电导钙离子激活钾通道电流和钙离子浓度变化

目的探讨糖尿病大鼠冠状动脉平滑肌细胞中大电导钙离子激活钾通道(BK通道)电流及钙离子浓度的变化。方法 40只SD大鼠随机均分为正常对照组(A组)和糖尿病组(B组)。采用链脲霉素腹腔内注射建立糖尿病大鼠模型,酶消化法分离冠状动脉平滑肌细胞,全细胞膜片钳实验和荧光测定方法分别检测冠状动脉平滑肌细胞BK通道电流和钙离子浓度。结果与A组相比,当刺激电压大于60mV时,B组冠状动脉平滑肌细胞BK通道电流密度明显下降(P<0.05);A组冠状动脉平滑肌细胞内钙离子浓度明显低于B组[(103±23)nmol/L vs.(193±22)nmol/L](P<0.05)。结论冠状动脉平滑肌细胞中BK通道电流下降及细胞内钙离子浓度升高可能是糖尿病冠状动脉功能损伤的重要原因。     

福辛普利对去窦弓神经大鼠肠系膜阻力血管结构改变的影响

目的:研究血管紧张素转换酶(ACE)抑制药福辛普利对去窦弓神经(SAD)大鼠肠系膜阻力血管结构改变的逆转作用。方 法:大鼠行SAD术后随机分为SAD组、福辛普利治疗组,另设假手术对照组,给药和(或)饲养16wk后处死大鼠,取肠系膜动脉二 级分枝,应用光镜和计算机图像分析技术观察组织病理学改变。结果:与SAD组大鼠相比,福辛普利治疗组大鼠肠系膜阻力血管的 壁厚、壁厚／内径比率、壁面积、平滑肌细胞核数／视野明显减小,而平滑肌相对面积比未发生显著改变。结论:福辛普利可明显抑制 SAD大鼠肠系膜阻力血管的结构改变。     

前列地尔治疗2型糖尿病合并颈动脉内膜增厚患者的心率变异性分析及临床意义

目的探讨前列地尔治疗2型糖尿病合并颈动脉内膜增厚患者的心率变异性分析及临床意义。方法选取2型糖尿病合并颈动脉内膜增厚患者121例,分为前列地尔脂微球载体注射液治疗组和丹参针治疗组,并与30例体检正常的正常组进行对照分析。观察治疗前后HolterHRV时域指标,评估心脏自主神经调节的功能。结果 2型糖尿病颈动脉内膜增厚组各HRV指标（SDNN,SDANN,RMSSD,PNN50,SDNN指数）均较正常组低（P均〈0.05）。前列地尔治疗前后各HRV指标有显著差异（P均〈0.05）。结论前列地尔治疗2型糖尿病合并颈动脉内膜增厚患者能改善其的自主神经调节功能。     

Renal dysfunction induced by long-term exposure to depleted uranium in rats

Depleted uranium (DU) is a kind of radioactive heavy metal which can enter into the body via inhalation (aerosols), ingestion (drinking and eating) and wounds (embedded), and causes chemical and/or radiation-induced toxicities. In this study, male Sprague Dawley rats were surgically implanted in gastrocnemius muscle with DU fragments at three dose levels (low-dose, medium-dose and high-dose), with biologically inert tantalum (Ta) fragments served as controls. At 1 day, 7 days, and 3, 6, and 12 months after implantation, the rats were euthanized and tissue samples were collected, and uranium levels were measured in a variety of tissues by inductively coupled plasma-mass spectrometry (ICP-MS) to analyze the dynamic changes and distribution of uranium in rats. Thereafter, at 3, 6 and 12 months after implantation, the rats were euthanized after the collection of 24 h urine, blood and kidney samples were collected for analysis of DU-induced renal histopathologic changes and renal dysfunction. It was observed that DU concentrations in all the DU implanted groups were higher than that in Ta control group, and DU concentrations in the kidney increased with the implanted times, peaked at the 90 days after implantation, with a high correlation to the implanted DU doses, and then began to decrease gradually and slowly, and the DU concentrations in kidney still maintained at a relatively high level even at the 360 days after implantation. Otherwise, chronic DU contamination could induce the pathological changes of renal glomeruli, tubules and mesenchyme, such as interstitial fibrosis, enlarged interstice of renal tubular epithelial cells, tumefactions and necrosis of epithelial cells, shrinkage and disappearance of cavity of Bowman’s capsule. By TEM, it was shown that the basement membrane of glomerulus was incrassated, mitochondrial of kidney proximal tubule had visible tumefaction and became bigger, and the mitochondrial cristae became shorter and disorderly in alignment. Compared to the control group, it was found that there was significant increase in the DU implantation group in terms of their blood urea nitrogen (BUN) and serum creatinine, urinary β2-microglobulin (β2-MG) and albumin, with a high correlation to the implanted DU dosage and periods. It was concluded that DU could accumulate in kidneys for a long period, and causes kidney injury by the toxic chemical/radioactive action such as renal dysfunction and structural damage.