脂多糖诱导的血管外膜炎症对兔股动脉内膜增生的影响及机制

通过用脂多糖诱导兔股动脉外膜炎症,来观察其对内膜增生的影响,并用免疫组织化学法观察股动脉壁核因子κB p65的表达情况,从而探讨外膜炎症对内膜增生影响的分子机制。高脂饮食饲养新西兰大耳白兔24只,两侧股动脉按实验要求分为分为脂多糖组(n=24)和对照组(n=24)。制备用脂多糖诱导的外膜炎症模型,于术后0天(n=8)、3天(n=8)和2周(n=8)处死动物取得股动脉标本,HE染色观察形态学变化和内膜增生情况,同时用免疫组织化学方法镜下观察核因子κB p65在动脉壁的表达。结果发现3天和2周时,脂多糖组血管外膜和内膜面炎症细胞明显增多。在3天时,脂多糖组血管内皮细胞和外膜细胞在胞浆中出现核因子κB p65阳性表达。计算机图象分析发现,2周时脂多糖组内膜面积(0.93±0.14mm2)和对照组(0.75±0.15mm2)相比有明显差异(P<0.05)。结果提示脂多糖诱导的血管外膜炎症可导致兔股动脉内膜增生,而在内膜增生之前伴随着血管内皮细胞和外膜细胞核因子κBp65的阳性表达,外膜炎症可能是通过激活上述细胞中的核因子κB从而启动炎性细胞因子的转录导致内膜增生。     

聚乳酸聚羟基乙酸共聚物涂层雷帕霉素洗脱支架对小型猪冠状动脉内膜增生的影响

目的:评价生物可降解的聚乳酸聚羟基乙酸共聚物(PLGA)涂层雷帕霉素洗脱支架对健康小型猪冠状动脉内膜增生的影响.方法:26只健康小型猪随机分入316L不锈钢裸金属支架组(316 L组)、L605钴铬合金裸金属支架组(L605组)、PLGA涂层L605支架组(PLGA组)和PLGA涂层雷帕霉素洗脱支架组(雷帕霉素组).各组均包括1周观察终点的猪1只和4周观察终点的猪5只.雷帕霉素组还包括12周观察终点的猪2只.每只猪于左前降支和右冠状动脉各置入同种支架1枚.至观察终点时复查冠状动脉造影并处死取材,通过形态学方法观察内膜增生情况.结果:4周时反映内膜增生的各项指标雷帕霉素组均显著优于其它3组,而其它3组之间没有显著性差异.雷帕霉素组与316L组相比支架上内膜厚度少73%(0.11 mm对0.41 mm),支架间内膜厚度少79%(0.06 mm对0.29 mm),新生内膜面积少69%(0.64 mm2对2.09 mm2),面积狭窄百分比少6l%(18.53%对47.27%).316L组有4例、L605组有3例发生支架内狭窄,而雷帕霉素组无支架内狭窄发生.12周时雷帕霉素组内膜增生有所加重,但较4周时相比除了支架间内膜厚度外其他反映内膜增生的各项指标差异均无统计学意义.结论:采用可降解的PLGA涂层雷帕霉素洗脱支架可以显著抑制健康小型猪冠状动脉支架置入术后4周和12周的内膜增生.     

新型血管内可吸收镁合金支架的实验研究

目的评估自行设计制作的新型血管内可吸收镁合金支架的生物相容性、有效性和安全性。方法杂种犬35只,每只犬均于冠状动脉和股动脉置入可吸收镁合金支架1枚,分别于术后1、3、5 d和1、2、3、4周,每个时间点5只犬,复查冠状动脉和股动脉,血管造影后取材,分离支架段血管行组织病理观察及计算机图像分析,测量内弹力板面积、管腔面积、内膜增生面积及内膜增生面积百分比。结果 51枚支架成功置入35只犬的冠状动脉和股动脉,各时间点冠状动脉及股动脉造影均证实管腔通畅,无狭窄病变,无血栓形成。组织病理显示,支架置入术后1、3、5 d无内膜增生,仍有支架残留;1周支架完全降解;2周开始出现内膜增生,3周至4周内膜增生相对明显。各时间点均未见明显炎性反应和血栓形成;术后2、3、4周,内膜增生面积分别为(0.04±0.03)mm~2,(0.10±0.03)mm~2,(0.15±0.04)mm~2;内膜增生面积百分比分别为(1.84±1.18)%,(3.72±1.12)%,(6.29±3.36)%,差异有统计学意义(P<0.05)。结论血管内可吸收镁合金支架具有良好的生物相容性,安全有效,易操作,再狭窄程度轻,临床应用前景好。     

外膜炎症诱发载脂蛋白E基因敲除鼠冠状动脉粥样硬化病灶

研究载脂蛋白E基因敲除(载脂蛋白E°)小鼠冠状动脉内粥样硬化病灶的分布、组成与动脉外膜炎症的关系.取载脂蛋白E°小鼠心脏作连续切片,Movat法染色,追踪冠状动脉主干及其心肌内的小分支;寻找病灶,观察病灶内组成,分析其分布规律.复制小鼠股动脉外膜无菌性炎症模型,用免疫组织化学方法检查内膜粘附分子的表达.结果发现,冠状动脉主干内有延伸病灶,在主干以下分支(包括心肌内小分支)内有在原位生成的病灶,在两类病灶相邻的外膜有炎性细胞浸润,外膜炎症面积大于动脉粥样硬化病灶累及的内膜面积,亦发现一些部位血管外有炎性细胞浸润,而尚无病灶形成.原位病灶均发生于心室壁,大的原位病灶多发生在左室壁心肌内、血管分支处和乳头肌附近的冠状动脉分支内.股动脉外膜炎症可诱发内膜表达细胞间粘附分子1和血管细胞粘附分子1,同时伴白细胞的附壁.以上提示血管外膜炎症是小鼠冠状动脉内病灶的一个始动环节.     

肝素与阿魏酸钠对自体移植静脉内膜增生的影响

目的:采用袖套法改良大鼠自体移植静脉内膜增生模型,观察肝素与阿魏酸钠对移植静脉内膜增生的影响,以减少再狭窄率,为防治桥管再狭窄提供理论依据。方法:采用袖套法将大鼠自体颈外静脉移植入同侧颈总动脉,分别给予肝素(800 U/kg,ip,bid)、阿魏酸钠(100 mg.kg-1.d-1,iv)及两者联合用药至术后2周。应用病理形态学方法通过计算机图像分析,观察术后各组大鼠移植静脉内膜增生情况及药物对其影响;应用增殖细胞核抗原(PCNA)免疫组织化学方法检测移植静脉血管平滑肌细胞(VSMC)中PCNA表达的变化。结果:阿魏酸钠组和阿魏酸钠加肝素组与移植对照组相比,移植静脉内膜增生程度显著减轻(均P<0.05),PCNA阳性细胞比例显著下降(均P<0.05);肝素组与移植对照组相比,移植静脉内膜增生受到一定的抑制,但差异无统计学意义,肝素组移植静脉PCNA阳性细胞比例与移植对照组相比差异无统计学意义。结论:阿魏酸钠能显著抑制移植静脉内膜增生,而肝素无显著抑制作用;袖套法静脉移植模型设计科学,手术操作简便,成功率高。     

L-精氨酸对糖尿病兔动脉损伤后内膜增生和内皮功能的影响

目的 :探讨糖尿病动脉损伤后内膜增生的机制和L 精氨酸对内膜增生及内皮功能的影响。方法 :2 8只糖尿病兔和 14只正常兔髂动脉行球囊损伤术后分为对照 (Con)组、糖尿病 (DM)组、L 精氨酸(L arg)组 ( 2 2 5 %L arg溶液饮水 )。术后 4周取髂动脉行图象分析或血管反应性测定 ,同时测定血浆中MDA、SOD和NO含量。结果 :DM组血浆中MDA水平明显低于Con组和L arg组 ,而SOD和NO水平明显降低。DM组内膜面积明显大于对照组 ( 0 2 5 5± 0 0 2 4vs.0 176± 0 0 2 9mm2 ,P <0 0 1) ,而L arg组内膜面积明显小于DM组 ( 0 15 3± 0 0 16,P <0 0 1)。L arg组髂动脉环对乙酰胆碱的舒张反应明显高于DM组。结论 :L arg能改善糖尿病兔的内皮功能 ,抑制动脉损伤后内膜增生     

氟伐他汀对动脉粥样硬化血管外膜炎症的影响

目的探讨氟伐他汀对实验性动脉粥样硬化(AS)家兔血管外膜炎症的影响及其机制。方法32只新西兰白兔随机分为3组:①对照组8只;②AS模型组12只;③氟伐他汀组12只,喂养12w后处死,取得主动脉标本,用HE染色观察形态学变化和血管外膜炎症细胞浸润情况,用免疫组化染色镜下观察血管外膜成纤维细胞NF-κBp65活性变化。结果正常对照组胸主动脉外膜未见炎性细胞浸润,成纤维细胞胞核内未见NF-κBp65阳性表达。AS组血管外膜可见明显的炎性细胞浸润,成纤维细胞胞核中NF-κBp65阳性表达明显增加。氟伐他汀组血管外膜可见炎性细胞浸润,但较AS组明显减少〔(0.17±0.02)与(0.43±0.19),P=0.003〕,成纤维细胞NF-κBp65有阳性表达,亦较AS组明显减少〔(0.31±0.02)与(0.57±0.04),P=0.002〕。结论氟伐他汀对AS血管外膜炎症的抑制作用可能与抑制成纤维细胞NF-κBp65活性有关。     

动脉损伤后血管外膜炎症细胞浸润及曲尼司特的干预效应

目的研究动脉内膜损伤后血管外膜炎症细胞的浸润,以及曲尼司特对上述指标的干预。方法球囊拉伤兔髂动脉内膜,随机分为对照组与曲尼司特组,在术后1 h、1 d3、d、7 d、14 d取髂动脉,通过组织学检查,免疫组化方法检测血管外膜炎症细胞的浸润及曲尼司特对它们的影响。结果(1)术后外膜可见T淋巴细胞出现,逐渐增高,于7 d达到最高峰,曲尼司特组较对照组无变化。(2)术后外膜见中性粒细胞、巨噬细胞、肥大细胞表达,均在3 d达到最高峰,曲尼司特组各时间点明显下降。结论(1)内膜损伤后,外膜炎症细胞浸润,以巨噬细胞、中性粒细胞为主(。2)曲尼司特降低血管各层增生,增加管腔面积,减少巨噬细胞、中性粒细胞、肥大细胞在血管外膜的浸润表达,对T淋巴细胞无影响。     

可降解雷帕霉素洗脱支架对猪冠状动脉支架置入术后内膜增生的影响

目的:考察可降解雷帕霉素洗脱支架对冠状动脉支架置入术后近期及远期内膜增生影响.方法:所有24只小型猪随机分为1个月及3个月两部分,每部分再随机分为A、B、C 3小组,每小组4只,分别于左冠状动脉前降支及右冠状动脉置入裸支架、聚合物洗脱支架及雷帕霉素洗脱支架,于术后1个月或3个月后动物处死前行冠状动脉造影,处死后用组织形态学方法观察内膜增生情况.结果:47枚支架均成功地置人24头小型猪的冠状动脉,术后均存活.术后即刻冠状动脉造影显示均通畅,处死前冠状动脉造影显示,1个月部分A组及B组各相关动脉均通畅,而C组有1支冠状动脉完全闭塞;3个月部分各动脉均通畅.形态学分析,与裸支架比较,1个月及3个月结果均显示聚乳酸洗脱支架对内膜增生无刺激作用;1个月结果显示药物支架可使管腔直径增加18.0%(P＜0.05),管腔面积增加22.6%(P＜0.05),面积狭窄百分比减少43%(P＜0.05),内膜面积减少35.1%(P＞0.05);3个月部分结果显示,药物洗脱支架对内膜增生的抑制作用消失,甚至有刺激内膜增生的趋势.结论:以聚乳酸为载体的可降解雷帕霉素洗脱支架在小型猪冠状动脉模型虽能抑制1个月血管内膜增生,但远期效果欠佳,其临床意义有待观察.     

雷帕霉素洗脱支架扩张程度对内膜增生影响的血管内超声研究

目的 观察冠状动脉内雷帕霉素洗脱支架扩张程度对内膜增生的影响.方法 对2002年4月至2005年3月73例冠心病患者置入雷帕霉素洗脱支架后8个月利用血管内超声测定支架近端、支架远端和支架内管腔最小处血管段外弹力膜（EEM）横截面积（CSA）、支架内CSA、管腔CSA、新生内膜面积、支架最大直径及最小直径,并推算支架对称指数.利用最小支架CSA与同一部位EEM CSA比值、最小支架CSA与支架两端CSA平均值比值、最小支架CSA和最小支架CSA处支架对称指数来判断支架扩张程度,并观察支架扩张程度对内膜增生的作用.结果 最小支架CSA/EEM CSA＜0.5 （n=56）与最小支架CSA/EEM CSA≥0.5（n=20）、最小支架CSA/支架两端CSA平均值＜0.9（n=44）与最小支架CSA/支架两端CSA平均值≥0.9（n=32）、最小支架CSA＜5 mm^2（n=25）与最小支架CSA≥5 mm^2（n=51）及对称指数＜0.9（n=37）与对称指数≥0.9（n=39）患者比较内膜增生差异无统计学意义.结论 雷帕霉素洗脱支架高压释放后支架扩张不全对支架内内膜增生没有影响.     

Effect of p53 deficiency on external vascular cuff-induced neointima formation.

The p53 tumor suppressor gene may act as an inhibitor of vascular neointima formation in response to injury and in the present study the effects of p53 deficiency on external vascular cuff-induced neointima formation were evaluated. Vascular neointima formation was induced by an external vascular cuff; a polyethylene tube placed around a 2 mm segment of the left femoral artery ensheathed the adventitia, but avoided direct intraluminal injury. Two weeks after cuff placement, the cuff-sheathed and contralateral control arteries without cuff from wild-type (n=10) and p53 deficient (n=8) mice were harvested and analyzed by quantitative morphometry. The areas of the lumen, intima, and media were measured in 10 cross-sections from one edge to the other of the cuffed portion, and in the corresponding 2-mm segment of the contralateral control artery. The volume ratio of the intima to media (I/M) was calculated. The contralateral control arteries without a cuff did not have intima in either wild-type or p53 deficient mice. In the cuff-sheathed arteries, neointima formation of p53 deficient mice with an I/M of 93% was significantly greater than that of wild-type mice with an I/M of 50% (P=0.001). The absence of p53 is associated with increased neointima formation in response to cuff injury.     

硝苯地平抑制核因子κB活性、改善鼠损伤血管炎症

目的 研究硝苯地平抑制损伤血管炎症反应的作用机制.方法 成年雄性C57BL/6J小鼠,10至12周龄,分为4组,即对照组(无手术无干预)、血管损伤组(只手术无干预)、硝苯地平1及5 mg·kg-1·d-1干预组(简称为硝苯地平1及5 mg干预组,手术+硝苯地平干预).另外,也检测了硝苯地平干预却未手术的小鼠的核因子κB(NF-κB)的表达,由于预测其结果与对照组相同,为免繁复,未单独设组.股动脉血管损伤手术后第5天采用Western blot检测NF-κB活性,第7天采用实时定量逆转录聚合酶链反应检测单核细胞趋化蛋白(MCP)-1 mRNA的表达、Western blot检测NF-κB的核转移.结果 术后第5天,血管损伤组、硝苯地平干预组NF-κB活性均显著高于对照组(P均＜0.05),硝苯地平5 mg干预组NF-κB活性显著低于血管损伤组(P＜0.05).术后第7天,血管损伤组、硝苯地平干预组MCP-1 mRNA表达显著上调[MCP-1 mRNA表达与GAPH的相对比率为:对照组0.0017±0.0001,血管损伤组0.0154±0.0002,硝苯地平1 mg干预组0.0120±0.0001,硝苯地平5 mg干预组0.0026±0.0001],血管损伤组、硝苯地平干预组MCP-1 mRNA表达均显著高于对照组(P均＜0.05),硝苯地平5 mg干预组MCP-1 mRNA表达显著低于血管损伤组(P＜0.05).术后第7天,血管损伤组、硝苯地平干预组细胞质中p50、IκBα及IκBβ蛋白水平显著下降[p50蛋白水平各组与对照组倍数比率为:对照组1.000±0.028,血管损伤组0.234±0.012,硝苯地平1 mg干预组0.303±0.014,硝苯地平5 mg干预组0.493±0.027.IκBot蛋白水平各组与对照组倍数比率为:对照组1.000±0.031,血管损伤组0.358±0.025,硝苯地平1 mg干预组0.373±0.029,硝苯地平5 mg干预组0.681±0.019.IκBβ蛋白水平各组与对照组倍数比率为:对照组1.000±0.022,血管损伤组0.483±0.047,硝苯地平1 mg干预组0.524±0.047,硝苯地平5 mg干预组0.723±0.031],血管损伤组、硝苯地平干预组细胞质中p50、IκBα及IκBβ蛋白水平均显著低于对照组(P均＜0.05),硝苯地平5 mg干预组细胞质中p50、IκBα及IκBβ蛋白水平均显著低于血管损伤组(P均＜0.05).血管损伤组、硝苯地平干预组细胞核内p50蛋白水平显著升高[p50蛋白水平各组与对照组倍数比率为:对照组1.000±0.031,血管损伤组24.608±1.078,硝苯地平1 mg干预组21.913±0.922,硝苯地平5 mg干预组6.522±0.504],血管损伤组、硝苯地平干预组细胞核内p50蛋白水平均显著高于对照组(P均＜0.05),硝苯地平5 mg干预组细胞核内p50蛋白水平显著低于血管损伤组(P＜0.05).结论 动脉血管损伤诱导血管炎症反应,硝苯地平抑制损伤动脉MCP-1表达,其可能是通过抑制NF-κB的DNA结合活性实现的,从而最终改善损伤血管的炎症反应.     

Early and late outcomes of percutaneous transluminal angioplasty of cephalad arteries

BACKGROUND: Efficacy of carotid endarterectomy (CEA) in prevention of stroke in patients with carotid artery stenosis has been confirmed in randomised trials. Carotid artery stenting (CAS) is a routine clinical practice and recent results of CAS are not worse than CEA. Moreover, percutaneous transluminal angioplasty (PTA) techniques allow other cephalad arteries to be dilated. AIM: To assess early and long-term outcome of PTA of cephalad arteries and to determine risk factors of early and late major adverse cardiovascular and cerebral events (MACCE). METHODS: The study group consisted of 223 consecutive patients (151 males, 67.7%, mean age 65.3+/-8.6) in whom 256 PTA procedures of cephalad arteries were performed. Two hundred and forty-two internal carotid, 7 common carotid and 15 vertebral arteries were dilated. Thirty-four patients underwent one-stage carotid and coronary procedures, while in 46 patients one-stage carotid and peripheral procedures were performed. Neuroprotection with a distal protection device was used in 51.5% of cases. The procedures were divided into two groups: with high (n=181) and low (n=75) risk of cardiovascular events. Early and late events were recorded and analysed subsequently. RESULTS: In hospital 30-day MACCE occurred in 12 (4.6%) patients, including 7 (2.7%) strokes, 3 (1.1%) myocardial infarctions and two (0.8%) deaths. Transient ischaemic attacks were observed in 8 patients, pulmonary oedema in 3 cases, as well as a single episode of retinal artery embolisation and acute renal insufficiency. The incidence of 30-day MACCE was not significantly higher in the high-risk group (6.07 vs. 1.33%; NS), but the risk of any adverse event was significantly higher (p=0.03). There was no difference in stroke incidence between procedures with or without neuroprotection (2.27 vs. 3.22%; NS). There was no difference in risk of MACCE between angioplasty of cephalad artery and one-stage cephalad and coronary artery angioplasty procedure (3.6 vs. 5.5%; NS). During 50.3+/-20 months of follow-up there were 16 (7.1%) deaths, 9 (3.5%) strokes and 6 (2.3%) re-stenoses confirmed angiographically. One-year total survival and one-year MACCE-free survival rates according to the Kaplan-Meier analysis were 94.9% and 89.0%, showing a trend towards better outcome in the low-risk group (F-Cox=2.46; p=0.19 and F-Cox=2.17; p=0.09 respectively). CONCLUSIONS: Percutaneous transluminal angioplasty of cephalad arteries is safe and feasible, with a low periprocedural complication rate and good late outcome. Carotid artery stenting is an alternative method to CEA.     

Stent Deployment Pressure Defines the Stent/Vessel Wall Relationship and has Important Implications for Early and Late Outcome

OBJECTIVE: This study evaluates the effect of stent deployment pressure on stent deployment, coronary vessel injury, subacute reclosure and foreign body reaction in a porcine coronary model. METHODS: Stainless steel coil stents were deployed in the right coronary artery of 30 pigs either using a deployment pressure of 4 atm (group I), 8 atm (group II), or 14 atm (group III). Serial quantitative angiographic studies together with morphometric analysis of the stented vessels were performed. RESULTS: Three pigs died within 48 hours due to subacute thrombosis (group I: n = 1, group II: n = 0, group III: n = 2). Another 4 stents were found occluded at day 7 (group I: n = 3, group II: n = 0, group III: n = 1). Imperfect stent alignment was found in 8 coronary arteries (group I: n = 7, group II: n = 1, group III: n = 0). Deep protrusion of stent filaments was found in 7 coronary arteries (group I: n = 0, group II: n = 1, group III: n = 6). Area stenosis at 6 weeks of the patent vessels was as follows: 75.7 +/- 15.2% in group I, 31.8 +/- 12.3% in group II, and 66.9 +/- 21.4% in group III, p < 0.001). CONCLUSION: In a porcine coronary model, stent deployment pressure resulting in an optimal alignment and a minimal coronary vessel injury leads to minimal neointimal hyperplasia.     

主动脉腔内修复术对B型主动脉夹层患者肾动脉血流及肾脏功能的影响

目的探讨主动脉腔内修复术对于B型主动脉夹层患者主动脉腔内修复术前、术后肾动脉血流及肾脏功能的影响。方法选择B型主动脉夹层患者110例,根据男性肾动脉受累类型不同分为ⅠA组(单侧或双侧肾动脉均为动力型缺血)10例、ⅠB组(单侧肾动脉为静力型缺血)36例、ⅠC组(双侧肾动脉为静力型缺血)8例;根据男性肾动脉受累数目分为双侧肾动脉未受累(未受累组)20例、单侧肾动脉受累(单侧受累组)38例、双侧肾动脉受累(双侧受累组)34例;根据女性肾动脉受累数目分为双侧肾动脉未受累(未受累组)8例、单侧肾动脉受累(单侧受累组)7例、双侧肾动脉受累(双侧受累组)3例。术前及术后观察双侧肾动脉的缺血情况及肾功能检查指标。并将各项指标进行对比。结果 220支肾动脉中动力型缺血共42支(19.1%);静力型缺血共80支(36.4%),主动脉腔内修复术后肾动脉动力型缺血全部得到显著改善,静力型缺血者可得到不同程度改善。随着肾动脉受累数量的增加,男性或者女性患者的肾功能受累情况呈进行性加重,且术后较术前呈下降趋势。结论对于B型主动脉夹层患者,主动脉腔内修复术能够开大主动脉真腔,提升肾动脉灌注,改善患者肾功能情况。     

Radial, carotid and aortic distensibility in congestive heart failure: effects of high-dose angiotensin-converting enzyme inhibitor or low-dose association with angiotensin type 1 receptor blockade

objectives; The aim of this study was to determine whether in patients with congestive heart failure (CHF) a distensibility (Dist) reduction: 1) similarly occurs in different arteries; 2) is related to CHF severity; and 3) is reversible with treatment. background: Several studies suggest that CHF is accompanied by a reduced arterial Dist. METHODS: We measured diameter in radial artery, carotid artery (CA) and abdominal aorta (AO) by echotracking. Distensibility was obtained by relating it to blood pressure. Data were collected in 30 patients with CHF (New York Heart Association functional class I to III) under standard treatment with diuretic, digitalis and angiotensin-converting enzyme (ACE) inhibitor in whom CHF severity was assessed by maximum oxygen consumption (VO(2)max) percentage and in 30 age- and gender-matched controls. Patients with CHF were then randomized to maintain standard treatment (n = 10), double the ACE inhibitor dose (n = 10) or add an angiotensin II antagonist (n = 10) and restudied after two months. RESULTS: Distensibility was markedly reduced in the CHF group in all three vessels (p < 0.01), CA and AO Dist being related to CHF severity (p < 0.05). After two months, Dist did not change in the group maintained under standard treatment, but it increased significantly (p < 0.05) and similarly when the ACE inhibitor dose was doubled or an angiotensin II antagonist was added. CONCLUSIONS: Congestive heart failure is characterized by a reduction of Dist of large-elastic and middle-sized muscular arteries. The reduction of large-elastic artery Dist is related to the CHF severity. These alterations can be reversed by drugs, effectively interfering with the renin-angiotensin system either at the ACE or at the angiotensin receptor level.     

慢性支气管炎与肺气肿大鼠肺血管炎症的实验研究

目的研究慢性支气管炎(CB)与肺气肿大鼠模型肺腺泡内动脉炎症反应特点及红霉素(EM)的干预作用。方法18只清洁级雄性Wistar大鼠按随机数字表法分为对照组(A组)、CB与肺气肿组(B组)及EM治疗组(C组),每组6只。采用气管内注入脂多糖(LPS)及烟熏法制作CB与肺气肿动物模型。8周后对大鼠肺脏进行病理学及形态学检测。结果(1)肺腺泡内动脉炎症反应表明,A组外膜面积炎性细胞总数为(33±6)个／mm2,B组为(158±68)个／mm2,C组为(54±7)个／mm2;A、B两组间及B、C两组间比较差异有统计学意义(t分别=9．6、9．2,P均<0．01);(2)肺腺泡内动脉病理图像分析显示,A组内膜面积/血管总面积为(21±4)％,B组为(37±3)％,C组为(30±1)％,B、C组与A组比较差异均有统计学意义(t分别=9．7、9．4,P均<0．01);(3)相关分析结果显示,肺腺泡内肌型动脉(MA)外膜炎性细胞总数与血管内膜厚度呈正相关(r=0．662,P<0．01)。结论CB组大鼠MA、非肌型动脉(NMA)和部分肌型动脉(PMA)存在以淋巴细胞为主的炎症反应,该炎症反应在肺血管重塑中起重要作用。EM对CB大鼠肺血管炎症及其重塑有较好的抑制作用。     

Flow-dependent dilatation of the cavernous artery. A potential test of penile NO content

BACKGROUND: Nitric oxide (NO) is now considered as the main contributor to elicit and maintain erection. It is also established that flow-dependent dilatation of conduit arteries is mediated by NO. The present study was designed to verify the possibility of assessing the penile NO content when measuring the post occlusive vasodilatation of the cavernous arteries.PATIENTS AND METHODS: Ninety five subjects, 22 with normal erections (control group) and 73 with various degrees of erectile dysfunction (ED), measured with the international index of erectile function (IIEF) and erectile activity index (IAE). Multidisciplinary evaluation helped to separate two subgroups: mainly organic (n=47) and mainly psychologic (n=26). The diameter of one of the two cavernous arteries was measured by duplex-scan before and after a five-minute complete occlusion of penile vascular flow. The criterion retained was the maximum percentage of dilatation achieved within 45 to 90 sec after the release of the occlusion. Means were compared in the clinical groups. Influences of IIEF, IAE, age, arterial risk factors, preocclusive diameter of the artery, testosterone and DHEA levels were evaluated.RESULTS: The mean percentage of increase in the control group was 65.2 +/- 26.3% vs 34.9 +/- 34.9% for the ED group (p=0.0003). The psychologic subgroup with 68.2 +/- 40% was similar to the control group as opposed to the organic group which showed a highly-significant difference (16.4 +/- 8.4; p=0.0001). In the control group and the psychological sub-group, subjects with arterial risk factors exhibited a less pronounced response (53.7 +/- 22) as compared to those free of any risk factors (80.3 +/- 30%) p=0.007. Age (r=0.29), preocclusion arterial diameter (r=0.3) and DHEA-S (r=0.56) as well as IIEF and IAE were correlated with the magnitude of the reaction. Sensitivity (100%) and specificity (92%) have been achieved in discriminating organic from psychologic DE.CONCLUSION: Flow-dependent vasodilatation of the cavernous artery is extremely strong. It is much stronger in control subjects and in patients with predominantly psychological ED. An increase of 30% seems to be a critical level since only patients in the organic group were below that level. Thus, organic ED seems to be linked to the decrease of NO production by the cavernous bodies. If these results were confirmed post occlusive vasodilatation of the cavernous artery might be proposed as a fully non-invasive diagnostic and prognostic test in the study of ED. We propose to call it PNORT (penile NO release test).     

吡格列酮对非糖尿病急性冠脉综合征患者炎症因子的影响

目的：探讨吡格列酮抑制非糖尿病急性冠脉综合征（ACS）患者动脉粥样硬化炎症的作用及可能机制。方法：将非糖尿病ACS患者随机分成吡格列酮组（40例，每日服吡格列酮15mg）和常规治疗组（42例）；另选20例健康者作为对照。分别于用药前、用药30天后抽取静脉血，用免疫散射比浊法和酶联免疫吸附法分别测定血清高敏C反应蛋白（hsCRP）和可溶性血管细胞粘附分子1（sVCAM-1）的浓度，并计算胰岛素抵抗指数（HOMA—R）。结果：用药前ACS患者hsCRP和sVCAM-1水平均高于正常对照组（P〈0．01）。用药30天后，ACS患者hsCRP和sVCAM-1水平明显下降（P〈0．01）;吡格列酮组hsCRP和sVCAM—1较常规治疗组下降更明显（P〈0．01）；吡格列酮组HOMA—R明显下降（P〈0．01），且hsCRP和sVCAM-1的下降与HOMA—R下降成正相关（r=0．47和0．39，P均〈0．01），血糖浓度略有下降，但差异无统计学意义。结论：吡格列酮可显著降低非糖尿病急性冠脉综合征患者血清炎症因子水平，抑制动脉硬化炎症反府；降低胰岛素抵抗是其可能机制之一。