Studies of autacoid responsiveness and endothelium dependency in human umbilical arteries

The effect of serotonin, prostaglandin E₂ (PGE2) and PGF_2α on the smooth muscle tension in perfused human umbilical arteries was investigated before and after removal of the endothelium. Denudation was performed mechanically using a nylon filament loop, and the efficiency of the procedure was checked by electron microscopy. In non-denuded vessels the autacoids elicited biphasic pressure responses, all starting with a vasodilatation and followed by a strong vasoconstriction. After denudation no dilatatory responses were evoked, whereas the constrictory responses appeared to be unchanged. Pre-treatment of the vessels with methylene blue did not affect the autacoid responses. Generally the perfusion pressure decreased after the de-endothelialization, in some preparations to levels of about 50% of the initial perfusion pressure. In about one-third of the preparations exposure to methylene blue led to a definite pressure increase. The results indicate that endothelium-derived factors are involved in the autacoid responses and also in the maintenance of basic vascular tonus in the umbilical circulation.     

Prevention of trypsin-induced shock in rats by the pancreatic secretory trypsin inhibitor

Jönsson P, Ljungcrantz I, Ohlsson K. Prevention of trypsin-induced shock in rats by the pancreatic secretory trypsin inhibitor. Scand J Clin Lab Invest 1994; 54: 595-9.

Intravenously infused bovine trypsin, 75mgkg^?l during 3h, induced shock in rats which proved lethal. After 5 h, all the rats had died. In another group of rats receiving trypsin, the pancreatic secretory trypsin inhibitor, 75 mg kg^?1, was infused during 5 h. These rats all survived. After about 1 h, α₁-macroglobulin was found to be saturated in both groups, while kininogen cleavage, coinciding with a decline in arterial blood pressure, only occurred in the untreated group. Trypsin complex formation with α₁ inhibitor 3 and α₁-proteinase inhibitor was more pronounced in untreated rats. It is concluded that the pancreatic secretory trypsin inhibitor may function as an effective trypsin inhibitor in plasma.     

乌司他丁对大鼠骨骼肌缺血-再灌注损伤的保护作用

目的 探讨乌司他丁对大鼠骨骼肌缺血-再灌注损伤的保护作用.方法 24只健康成年雄性SD大鼠随机分为3组(每组8只):对照组(C组)、缺血.再灌注损伤组(I/R组)、乌司他丁处理组(U组).C组仅麻醉肢体没有缺血操作;I/R组于再灌注前颈外静脉注入生理盐水0.5 ml;U组于再灌注前同法给乌司他丁0.5 ml(5×104 U/kg).以橡皮带环绕结扎大鼠左后肢根部至趾掌无血流信号达4 h后放开橡皮带,再灌注4 h建立大鼠骨骼肌缺血.再灌注损伤模型.再灌注4 h各组处死动物采集标本,采用逆转录-聚合酶链反应(RT-PCR)法测定骨骼肌组织TNF-α mRNA的表达;酶联免疫吸附试验法(ELISA)测定血浆TNF-α水平;比色法检测血浆乳酸脱氢酶(LDH)、肌酸激酶(CK)、丙二醛(MDA)和组织过氧化物酶(MPO)含量,测定湿质量/干质量均(W/D)及光镜、电镜观察骨骼肌组织结构的变化.应用SPSS 10.0统计软件,用单因素方差分析.结果 骨骼肌组织TNF-α mRNA的表达在I/R组明显高于C组(P＜0.05),而U组则低于I/R组(P＜0.01);血浆TNF-α浓度I/R组明显高于C组(P＜0.01),而U组则低于I/R组(P＜0.05);血浆LDH、MDA、CK和组织MDA、MPO水平以及W/D比值I/R组高于C组(P＜0.05),U组则低于L/R组(P＜0.05);骨骼肌组织形态学和超微结构的损伤U组也较I/R组减轻.结论 乌司他丁通过抑制细胞因子的生成、抑制氧自由基代谢产物MDA的产生和减少MPO的活性而对骨骼肌缺血-再灌注起保护作用.     

Atherosclerosis and thromboembolic risk in atrial fibrillation: Focus on peripheral vascular disease

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. It results in a 5-fold increased risk for stroke and thromboembolism and is associated with a high morbidity and mortality. AF shares several risk factors and pathophysiological features with atherosclerosis. Hence AF is often complicated by a variety of other cardiovascular conditions. Indeed, peripheral vascular disease (PVD) is highly prevalent among AF patients and associates with increased mortality. Inclusion of PVD within stroke risk scoring systems such as the CHA₂DS₂-VASc score improves risk stratification of AF patients. Of note, PVD has not been previously well documented nor looked for in observational studies or clinical trials. The aim of this present review article is to provide an overview of the association between atherosclerosis (with particular focus on PVD) and AF as well as its complications.     

Application of vascular endothelial cells in stem cell medicine

Stem cell medicine is gaining momentum in the development of therapy for various end-stage diseases. The search for new seed cells and exploration of their application prospects are topics of interest in stem cell medicine. In recent years, vascular endothelial cells (VECs) have attracted wide attention from scholars. VECs, which form the inner lining of blood vessels, are critically involved in many physiological functions, including permeability, angiogenesis, blood pressure regulation, immunity, and pathological development, such as atherosclerosis and malignant tumors. VECs have significant therapeutic effects and broad application prospects in stem cell medicine for the treatment of various refractory diseases, including atherosclerosis, myocardial infarction, diabetic complications, hypertension, coronavirus disease 2019, and malignant tumors. On the one hand, VECs and their extracellular vesicles can be directly used for the treatment of these diseases. On the other hand, VECs can be used as therapeutic targets for some diseases. However, there are still some obstacles to the use of VECs in stem cell medicine. In this review, advances in the applications and challenges that come with the use of these cells are discussed.     

谷氨酰胺对脓毒症大鼠肺血管内皮细胞的作用

目的 观察脓毒症大鼠肺血管内皮细胞(vascular endothelial cell,VEC)、细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)和E-选择素的变化特点并探讨谷氨酰胺对其的作用.方法 将Sprague-Dawley(SD)大鼠56只随机分成对照组、脓毒症组和治疗组.实验地点在中山大学北校区动物实验中心.脓毒症组注射脂多糖4mg/kg制备大鼠脓毒症模型,治疗组注射脂多糖4mg/kg和谷氨酰胺0.3g/kg,对照组不注射脂多糖.造模成功后,在6,12,24 h时间点分离大鼠肺标本,采用逆转录聚合酶链反应和免疫组织化学方法研究肺ICAM-1和E-选择素的表达;用Hoechest染色评价肺VEC凋亡;用电子显微镜观察肺VEC.采取SPSS 13.0软件包进行统计学处理,统计分析方法采用方差分析法.结果 脓毒症组大鼠肺ICAM-1和E-选择素的表达与治疗组和对照组比较明显增加(P＜0.01),治疗组ICAM-1蛋白和E-选择素的表达明显高于对照组(P＜0.05).脓毒症组和治疗组ICAM-1的表达24 h达到高峰,E-选择素的表达6 h达高峰.脓毒症组大鼠肺VEC凋亡明显多于治疗组(P＜0.05)和对照组(P＜0.01);治疗组大鼠VEC凋亡明显多于对照组(P＜0.01).电子显微镜观察也得到证实.结论 脓毒症大鼠肺ICAM-1和B选择素的表达明显增加,导致肺VEC的坏死和凋亡以及急性肺损伤的发生.谷氨酰胺对其有保护作用.     

螺内酯对心力衰竭患者血管内皮功能的影响

目的 研究醛固酮拮抗剂-螺内酯对纽约心脏病协会(NYHA)分级Ⅱ-Ⅳ级慢性心力衰竭(CHF)患者血管内皮功能的影响.方法 选择148例CHF患者,分为螺内酯治疗组77例与常规治疗组71例,比较两组患者于入选时及治疗6个月时肱动脉反应性充血管径变化(FMD).结果 在NYHA分级Ⅱ级、Ⅲ级、Ⅳ级的CHF患者均较正常对照组反应性充血时内径舒张率降低(P＜0.01);常规治疗组NYHAⅡ、Ⅲ级CHF患者治疗后反应性充血时内径舒张率较治疗前增加(P＜0.05～0.01);螺内酯治疗组NYHAⅡ级、Ⅲ级、Ⅳ级心力衰竭患者均较治疗前增加反应性充血时内径舒张率(P＜0.05～0.01),同时较常规治疗组显著增加反应性充血时内径舒张率(P＜0.01).结论 CHF患者均存在血管内皮功能障碍;以常规治疗基础上应用螺内酯治疗后对于NYHAⅡ级、Ⅲ级、Ⅳ级各级心力衰竭患者均能显著增加,FMD进一步改善血管内皮功能,而在慢性心力衰竭的的治疗过程中起着重要作用.提示螺内酯除了可以用于治疗重度心力衰竭(NYHAⅣ级),用于治疗轻中度心力衰竭(NYHAⅡ级、Ⅲ级)可以同样获益.     

康复训练对血管性痴呆大鼠学习记忆能力及海马区神经细胞黏附因子表达的影响

目的 探讨康复训练对血管性痴呆(VD)大鼠学习记忆的功能恢复及海马区神经细胞黏附因子(NCAM)表达的影响.方法 选择SD雌性大鼠45只,随机分为康复组20只、制动组20只和假手术组5只,采用双侧颈总动脉反复缺血再灌注加降血压法制作VD大鼠模型.3组分别于术后第27,28天以水迷宫试验评价大鼠学习记忆能力,采用核糖核酸逆转录聚合酶链反应(RT-PCR)法检测不同时间点海马区NCAM的表达.结果 水迷宫试验结果 显示,康复组学习记忆能力优于制动组,康复组NCAM在海马区的表达在术后第1天达到高峰,在第7,14天时间点康复组较制动组和假手术组均有明显增加.结论 康复训练可改善VD大鼠空间学习记忆能力,其分子机制可能与其海马上NCAM的表达水平的增高有关.     

康复训练对血管性痴呆大鼠学习记忆能力及海马区神经细胞黏附因子表达的影响

目的 探讨康复训练对血管性痴呆(VD)大鼠学习记忆的功能恢复及海马区神经细胞黏附因子(NCAM)表达的影响.方法 选择SD雌性大鼠45只,随机分为康复组20只、制动组20只和假手术组5只,采用双侧颈总动脉反复缺血再灌注加降血压法制作VD大鼠模型.3组分别于术后第27,28天以水迷宫试验评价大鼠学习记忆能力,采用核糖核酸逆转录聚合酶链反应(RT-PCR)法检测不同时间点海马区NCAM的表达.结果 水迷宫试验结果 显示,康复组学习记忆能力优于制动组,康复组NCAM在海马区的表达在术后第1天达到高峰,在第7,14天时间点康复组较制动组和假手术组均有明显增加.结论 康复训练可改善VD大鼠空间学习记忆能力,其分子机制可能与其海马上NCAM的表达水平的增高有关.     

康复训练对血管性痴呆大鼠学习记忆能力及海马区神经细胞黏附因子表达的影响

目的 探讨康复训练对血管性痴呆(VD)大鼠学习记忆的功能恢复及海马区神经细胞黏附因子(NCAM)表达的影响.方法 选择SD雌性大鼠45只,随机分为康复组20只、制动组20只和假手术组5只,采用双侧颈总动脉反复缺血再灌注加降血压法制作VD大鼠模型.3组分别于术后第27,28天以水迷宫试验评价大鼠学习记忆能力,采用核糖核酸逆转录聚合酶链反应(RT-PCR)法检测不同时间点海马区NCAM的表达.结果 水迷宫试验结果 显示,康复组学习记忆能力优于制动组,康复组NCAM在海马区的表达在术后第1天达到高峰,在第7,14天时间点康复组较制动组和假手术组均有明显增加.结论 康复训练可改善VD大鼠空间学习记忆能力,其分子机制可能与其海马上NCAM的表达水平的增高有关.     

康复训练对血管性痴呆大鼠学习记忆能力及海马区神经细胞黏附因子表达的影响

目的 探讨康复训练对血管性痴呆(VD)大鼠学习记忆的功能恢复及海马区神经细胞黏附因子(NCAM)表达的影响.方法 选择SD雌性大鼠45只,随机分为康复组20只、制动组20只和假手术组5只,采用双侧颈总动脉反复缺血再灌注加降血压法制作VD大鼠模型.3组分别于术后第27,28天以水迷宫试验评价大鼠学习记忆能力,采用核糖核酸逆转录聚合酶链反应(RT-PCR)法检测不同时间点海马区NCAM的表达.结果 水迷宫试验结果 显示,康复组学习记忆能力优于制动组,康复组NCAM在海马区的表达在术后第1天达到高峰,在第7,14天时间点康复组较制动组和假手术组均有明显增加.结论 康复训练可改善VD大鼠空间学习记忆能力,其分子机制可能与其海马上NCAM的表达水平的增高有关.     

康复训练对血管性痴呆大鼠学习记忆能力及海马区神经细胞黏附因子表达的影响

目的 探讨康复训练对血管性痴呆(VD)大鼠学习记忆的功能恢复及海马区神经细胞黏附因子(NCAM)表达的影响.方法 选择SD雌性大鼠45只,随机分为康复组20只、制动组20只和假手术组5只,采用双侧颈总动脉反复缺血再灌注加降血压法制作VD大鼠模型.3组分别于术后第27,28天以水迷宫试验评价大鼠学习记忆能力,采用核糖核酸逆转录聚合酶链反应(RT-PCR)法检测不同时间点海马区NCAM的表达.结果 水迷宫试验结果 显示,康复组学习记忆能力优于制动组,康复组NCAM在海马区的表达在术后第1天达到高峰,在第7,14天时间点康复组较制动组和假手术组均有明显增加.结论 康复训练可改善VD大鼠空间学习记忆能力,其分子机制可能与其海马上NCAM的表达水平的增高有关.     

康复训练对血管性痴呆大鼠学习记忆能力及海马区神经细胞黏附因子表达的影响

目的 探讨康复训练对血管性痴呆(VD)大鼠学习记忆的功能恢复及海马区神经细胞黏附因子(NCAM)表达的影响.方法 选择SD雌性大鼠45只,随机分为康复组20只、制动组20只和假手术组5只,采用双侧颈总动脉反复缺血再灌注加降血压法制作VD大鼠模型.3组分别于术后第27,28天以水迷宫试验评价大鼠学习记忆能力,采用核糖核酸逆转录聚合酶链反应(RT-PCR)法检测不同时间点海马区NCAM的表达.结果 水迷宫试验结果 显示,康复组学习记忆能力优于制动组,康复组NCAM在海马区的表达在术后第1天达到高峰,在第7,14天时间点康复组较制动组和假手术组均有明显增加.结论 康复训练可改善VD大鼠空间学习记忆能力,其分子机制可能与其海马上NCAM的表达水平的增高有关.     

Therapeutic ultrasound enhances medial collateral ligament repair in rats

The purpose of this study was to evaluate the effects of therapeutic ultrasound (US) on medial collateral ligament healing. A total of 36 3-month-old male Sprague-Dawley rats with transected medial collateral ligaments were studied. Subjects were given 5-min pulsed US therapy (duty cycle; one application in 4 ms; 1:4) daily with different durations (1 day, 5 days and 10 days) and intensities (0, 0.5 and 2.3 W/cm2). After each treatment, the level of transforming growth factor beta-1 (TGF-beta1) of the ligament was measured. TGF-beta1 was not detected in the 1-day group. In the 5-day and 10-day groups, the levels of TGF-beta1 were significantly up-regulated in the high-dose subgroup (p < 0.05). The 10-day group also registered a significantly higher expression of TGF-beta1 than did the 5-day group (p < 0.05). The present findings suggest that pulsed US therapy may enhance ligament repair by up-regulating the extent of TGF-beta1 in a high-dose application. Long-term treatment with this therapy could obtain further improvement.     

携GL-7靶向微泡造影剂对高脂饮食兔腹主动脉内膜的靶向作用

目的 探讨携GL-7靶向微泡造影剂对高脂饮食兔腹主动脉内膜体外特异性结合及体内增强显影效果.方法 14只新西兰兔用高脂饮食法建立腹主动脉内膜损伤模型,并随机分为两组,4周后分别使用对照微泡和靶向微泡造影剂进行腹主动脉超声造影,以视频密度法评价两种造影剂对动脉内膜的增强效果,荧光显微镜观察两种造影剂体内结合情况及与动脉内膜荧光染色的结合情况及荧光强度统计分析.结果 对照微泡、靶向微泡造影后血管内膜回声均较造影前增强,靶向微泡造影与对照微泡造影比较,血管内膜峰值视频密度差异有统计学意义(P<0.05).荧光显微镜观察,靶向微泡血管腔内呈现绿色荧光,而对照微泡血管腔内仅有微弱的绿色荧光.动脉血管冰冻切片结果显示,靶向微泡造影组动脉内膜有绿色荧光表达,而对照微泡造影组绿色荧光表达较弱,两组荧光强度差异有统计学意义(P<0.05).结论 GL-7靶向微泡造影剂与兔动脉血管内膜体内、体外特异性结合,可显著增强兔腹主动脉内膜靶向显影.     

山莨菪碱对小型猪缺血/再灌注心肌的保护作用

目的 探讨山莨菪碱对小型猪缺血／再灌注心肌的保护作用。方法12头小型猪，随机分为生理盐水组（6头）和山莨菪碱组（6头），球囊闭塞左前降支（LAD）造成心肌缺血，撤除球囊恢复冠脉再灌注，同时冠脉内注入药物后，测定血管内皮功能相关因子的变化。监测血压（MBP）、心率、平均冠脉内压（MICP），并在完成上述测定后，测量缺血和梗死心肌范围。结果①小型猪缺血／再灌注后，生理盐水组一氧化氮（NO）降低、内皮素（ET-1）和血小板聚集率（PagT）升高（P（0．05）；山莨菪碱组N0降低、ET-1和PagT升高（P〈0．05）。但升高的峰值变化与生理盐水组相比，幅度均明显减小，两组相比有显著性差异（P〈0．05）。②在冠脉内注射生理盐水后，MBP、MICP及心率均无明显变化（P〉0．05）；但在冠脉内注射山莨菪碱后，出现MBP、MICP及心率的升高，其最大变化发生在30min时（P〈0．05），并且与生理盐水组比较，冠脉内压明显升高（P〈0．05）。③山莨菪碱组缺血面积和梗死面积均显著小于生理盐水组（P〈0．01）。结论小型猪冠脉内注射山莨菪碱在缺血／再灌注后可保护血管内皮功能，抑制血小板积聚，增加冠脉灌注压，从而减少心肌的缺血和坏死面积。     

核因子κB的反义寡核苷酸对肿瘤坏死因子α诱导的血管细胞黏附分子-1表达的影响

目的：探讨人脐静脉内皮细胞（HUVECs）ECV304细胞株中，核因子κB（NF—κB）的反义寡核苷酸（AODNs）对肿瘤坏死因子α（TNF—α）诱导血管细胞黏附分子（VCAM-1）表达的影响。方法：将培养的人脐静脉内皮细胞株ECV304分为3组，其中2组用脂质体介导法转染寡核苷酸（ODNs）分别转染AODNs、正义寡核苷酸（SODNs）：另1组（阳性对照组）不转染ODNs。流式细胞仪荧光活细胞计数检测转染效率及NF-κB的表达情况，逆转录-聚合酶链反应、流式细胞仪检测及免疫组织化学染色测定AODNs对TNF—α诱导的VCAM—1表达的影响。结果：脂质体介导的转染方法能将ODNs有效地转染至HUVECs中，且AODNs可有效抑制NF-κB的复制合成。NF—κBP65的AODNs可使TNF—α刺激的人脐静脉内皮VCAM-1mRNA表达下调33．08％，蛋白质水平的表达下调48．27％，并与免疫组织化学染色显示结果一致。结论：NF—κB的AODNs可显著下调NF—κB调控的、与动脉粥样硬化相关的黏附分子表达。     

湖南地区成人血清IgG亚类水平调查及影响因素分析

目的调查湖南地区成年人血清IgG亚类的浓度水平,探讨年龄、性别及生活方式等因素的影响。方法用免疫散射比浊法测定170例体检者血清中IgG_1、IgG_2、IgG_3、IgG_4和IgG浓度。结果血清IgG_1、IgG_2、IgG_3、IgG_4和IgG浓度分别为(7.53±0.14)g/L、3.99(3.13,5.02)g/L、0.49(0.30,0.70)g/L、0.53(0.26,0.93)g/L、12.2(10.5,14.1)g/L;血清IgG_1/IgG、IgG_2/IgG、IgG_3/IgG和IgG_4/IgG分别为(61.3±0.69)%、33.38(27.8,38.8)%、3.97(2.5,5.3)%和4.44(2.1,7.3)%。女性血清IgG_3浓度及IgG_3/IgG比值高于男性(P=0.005,0.014);不同性别间IgG_1、IgG_2、IgG_4及IgG_1/IgG、IgG_2/IgG、IgG_4/IgG的差异无统计学意义。31~40岁组血清IgG_3浓度显著高于41~50岁组(P=0.03),而年龄对血清IgG_1、IgG_2和IgG_4浓度的影响无统计学意义。重度吸烟组血清IgG_1的浓度比不吸烟组低,差异有统计学意义(P=0.023)。重度吸烟组IgG_4/IgG高于不吸烟组(P=0.018)。中/重度饮酒组血IgG_1、IgG_3浓度和IgG_3/IgG比值比不饮酒组低(P=0.05,0.004,0.015)。代谢综合征低风险组血清IgG_3和IgG_3/IgG高于高风险组(P=0.034,0.038)。结论性别和年龄对于血清IgG_3浓度的影响有显著意义。重度吸烟可能导致IgG_1的浓度降低和IgG_4/IgG比值的上升。血清IgG_1、IgG_3和IgG_3/IgG的降低与饮酒存在一定的关系。     

Protective effects of liposomes encapsulating ferulic acid against CCl4-induced oxidative liver damage in vivo rat model

Antioxidants are useful for the treatment of oxidative stress mediated liver damage. A naturally occurring antioxidant γ-oryzanol is rapidly hydrolyzed to its active hydrophobic metabolite, ferulic acid, inside the body. Limitations associated with the hydrophobicity of ferulic acid can be overcome by encapsulating in a liposomal formulation. As intravenously administered nanoparticles (including liposomes) can effectively reach the liver, such systems may be suitable drug delivery carriers to treat liver injury. In this study, we prepared a liposomal formulation of ferulic acid (ferulic-lipo) and examined its effects on liver damage induced by CCl₄. Ferulic-lipo were ~100 nm in size and drug encapsulation efficiency was about 92%. Ferulic-lipo showed potent scavenging efficacy against hydroxyl radical compared to α-tocopherol liposomes. Ferulic-lipo significantly prevented CCl₄-mediated cytotoxicity in human hepatocarcinoma cells. Furthermore, intravenous administration of ferulic-lipo significantly reduced alanine aminotransferase and aspartate amino transferase levels in a rat model of liver injury. CCl₄-mediated reactive oxygen species generation in liver was also reduced by intravenous administration of ferulic-lipo. Hepatoprotective effects of ferulic-lipo were demonstrated by histological observation of CCl₄-induced liver tissue damage. Therefore, ferulic-lipo exhibit potent antioxidative capacity and were suggested to be an effective formulation for prevention of oxidative damage of liver tissue.     

Outbreak by meropenem-resistant Pseudomonas aeruginosa producing IMP-6 metallo-beta-lactamase in a Korean hospital

Pseudomonas aeruginosa isolates containing the bla(IMP-6) gene were recovered from 5 patients hospitalized at a tertiary-care hospital in Korea. The bla(IMP-6) gene was in a class 1 integron containing 5 different insert gene cassettes. All of the isolates showed identical pattern in SpeI macrorestriction analysis.