心肌炎分类方法颇多，病毒性心肌炎（ VMC ）是最常见类型。在20世纪90年代，随着聚合酶链反应（ PCR）及原位杂交法等分子生物学的发展，大大提高了诊断VMC特定病原体的能力。 VMC临床表现可从无临床症状到心律失常、心源性休克、心力衰竭，甚至猝死轻重不一，易于误诊。<br>　　1发病机制<br>　　VMC为病毒引起的自身免疫性疾病，可发展至扩张型心肌病〔1〕。在病毒感染的第一期，随着心肌细胞的溶解出现病毒血症，继而激活包括自然杀伤细胞、γ干扰素和一氧化氮等一系列固有免疫反应，随后抗原提呈细胞吞噬释放的病毒颗粒及心脏蛋白质，并将其移出到局部的淋巴结，大多数病人会在此阶段痊愈，仅有一小部分会进展到第二阶段-心肌损伤阶段，在此阶段，特异性T细胞和抗体指向病毒和肌球蛋白、β1受体（抗心肌抗体）等心脏表位物质，而导致一个强大的炎性反应〔2，3〕。对于其中大多数病人，病原体能够被清除及免疫反应下调，只有极少数患者病毒感染和炎症反应会持续存在，并进展到炎症性心肌病，它是扩张型心肌病的一种类型。通过长期随访VMC患者，发现近21％的患者发展为扩张型心肌病〔4〕，并且通过PCR技术检测到病毒基因组的心肌炎患者中有67％出现自发性的左心室功能减退〔5〕，可见扩张型心肌病是心肌感染后的晚期阶段。从急性心肌炎到扩张型心肌病，多种作用机制被提出，但自身免疫反应是公认导致心肌严重损伤的决定性因素。 Bowles等〔6〕通过对1988年到2000年间的624个感染心肌炎患者的活体组织切片分析，发现腺病毒成为最常见病原体，尤其多见于儿童〔5〕。细小病毒B19是最常见的病原体，通过损伤心肌内皮细胞常引起类心肌梗死样的心肌炎，表现为剧烈的胸痛，心电图ST-T段改变和血清肌钙蛋白I和T的明显升高。丙型肝炎病毒及甲型 H1 N1病毒引发的急性心肌炎也常有报道。

慢性充血性心力衰竭是胸腔积液的常见原因，而且部分患者以胸腔积液为首发症状。随着人口老龄化，糖尿病、心血管疾病的增多，老年人心源性胸腔积液的发生呈增多趋势，且易被误诊、误治。若不能做出迅速、正确的诊断，患者将要面临不必要的检查及治疗，增加经济负担，延误最佳治疗时机。

<正>替米沙坦属于非肽类血管紧张素Ⅱ(AngⅡ)受体拮抗剂(ARB),在AngⅡ1型受体(AT1R)水平同时阻断了肾素-血管紧张素系统(RAS)及非经典途径产生的AngⅡ的作用,降压效果更好,对其他激素无影响,清除半衰期为24 h,降压疗效较持久〔1〕。另外,替米沙坦分子结构与过氧化物酶体增殖物激活受

目的研究内皮型一氧化氮合酶(eNOS)基因导入对高血压大鼠心脏、肾脏细胞凋亡的影响。方法将实验大鼠分为自发性高血压大鼠(SHR)组、AAV-LacZ组和AAV-eNOS组,每组8只,另设8只正常血压(WKY)大鼠为WKY组。AAV-eNOS组经尾静脉注射AAV-eNOS 200μl(含eNOS基因拷贝1×1012),AAV-LacZ组注射AAV-LacZ 200μl,WKY及SHR组大鼠分别经尾静脉给予等量0.1 mol/L PBS。应用原位末端标记(TUNEL)法检测各组大鼠心、肾组织中的细胞凋亡,免疫组织化学方法检测eNOS的表达。结果①SHR组大鼠心肌组织及肾脏组织染色阳性信号明显增多,与WKY组比较具有显著性差异(P<0.05),AAV-eNOS组凋亡阳性信号明显低于SHR组,差异显著(P<0.05)。②SHR组及AAV-LacZ组大鼠心肌组织eNOS表达低于WKY组,差异具有显著性(P<0.05);与SHR组大鼠比较,AAV-eNOS组eNOS表达明显增加,差异具有显著性(P<0.05)。各组大鼠肾脏eNOS蛋白表达未见明显差异。结论 eNOS基因导入可明显抑制心肌及肾脏组织细胞的凋亡,保护靶器官。

目的探讨高血压患者血清脂联素(APN)水平变化与左心室肥厚(LVH)、颈动脉粥样硬化(CAS)的关系。方法将原发性高血压患者(121例)分为单纯高血压组(80例)和高血压合并LVH组(41例),另选同期健康体检者(35例)为对照组。根据颈动脉彩超结果,将所有高血压患者分为颈动脉斑块组、颈动脉内中膜(IMT)增厚组和颈动脉正常组。酶联免疫分析法测定血清APN水平。结果 (1)高血压合并LVH组血清APN浓度〔(5.43±0.89)μg/ml)〕明显低于对照组〔(13.06±1.06)μg/ml〕和单纯高血压组〔(7.52±0.65)μg/ml〕(均P<0.05)。(2)颈动脉斑块组血清APN浓度明显低于IMT增厚组和颈动脉正常组,分别为(5.37±1.78)μg/ml、(7.89±0.65)μg/ml和(10.16±1.45)μg/ml(P<0.05)。(3)相关分析显示,血清APN水平与左心室质量指数(LVMI)、内中膜厚度均呈现明显的负相关(r分别为-0.850、-0.376,均P<0.05)。结论 APN水平降低可能促进高血压患者左心室肥厚及颈动脉粥样硬化的发生与发展。

<正>不对称二甲基精氨酸(ADMA)是精氨酸甲基化衍生物,由甲基化蛋白生理降解而成。ADMA是主要的内源性一氧化氮合酶(NOS)抑制剂,该酶为合成一氧化氮(NO)所需,具有重要的抗动脉粥样硬化特性。血浆ADMA浓度升高会造成NO合成受损,导致血管内皮功能障碍和动脉粥样硬化性血管疾病。

目的探讨左旋氨氯地平联合培哚普利治疗老年原发性高血压(EH)合并左室肥厚(LVH)患者的临床效果。方法将80例EH伴LVH患者随机分为两组(年龄均≥60岁),对照组40例,治疗组40例。两组均给予苯磺酸左旋氨氯地平(施慧达,吉林天风制药公司)2.5～5 mg,1次/d;治疗组联合培哚普利(雅施达,天津施维雅制药公司)4～8 mg,1次/d,晨起顿服。治疗24 w,观察降压疗效和LVH改善情况。结果两组均能有效降低血压,逆转左室肥厚。治疗组降压总有效率95%,对照组82.5%,治疗组血压下降显著,两组间差异有显著性(P<0.05);治疗组左室舒张末期室间隔厚度(IVST)、左室后壁舒张末期厚度(LVPWT)及左室心肌重量指数(LVM I)均较对照组改善显著,差异均有显著性(P<0.05)。结论两药联合服用对老年EH伴LVH有协同逆转作用,可作为治疗EH伴LVH患者尤其是老年人的一线用药。

<正>糖尿病是大多数国家的主要死亡原因,通过增加如冠心病和周围血管疾病、中风、失明和肾衰竭等疾病的风险,而显著增加社会、家庭及经济负担。2006年联合国大会宣布2型糖尿病成为第一大非传染性疾病,与传染性疾病,如艾滋病和结核病一样严重威胁着全球人类的健康〔1〕。2型糖尿病的危险因素包括肥胖,缺乏身体活动和不健康饮食。2型糖尿病在不同社

目的观察丹蒌片对异丙肾上腺素所致大鼠急性心肌缺血损伤的保护作用。方法一次性多点皮下注射异丙肾上腺素(ISO,15 mg/kg)制备大鼠急性心肌缺血模型,并观察心电图J点、血清酶学、心肌病理形态及心肌坏死面积变化。结果丹蒌片能明显对抗心肌缺血大鼠心电图J点下移,降低血清CK、LDH和AST活性,改善心肌缺血引起的心肌组织病理损伤,缩小心肌坏死面积。结论丹蒌对大鼠急性心肌缺血具有明显的保护作用。

<正>高血压是严重危害人体健康和生活质量的疾病,是心力衰竭、脑卒中、终末期肾病和外周血管疾病的最重要高危因素之一。尽管高血压药物治疗得到长足

目的 通过应用替米沙坦治疗老年高血压伴胰岛素抵抗(IR)患者,观察其对超敏C反应蛋白(hs-CRP)水平变化及对胰岛素敏感性的影响.方法 老年高血压病伴IR患者60例,随机分为替米沙坦组和硝苯地平组各30例,治疗4 w,测定治疗前后血压、空腹血糖、真胰岛素、hs-CRP、血脂、血尿酸和IR指数、胰岛β细胞功能指数.结果 两组基线资料相匹配.替米沙坦组治疗后血压、真胰岛素、hs-CRP及HOMA-IR和HOMA-islet指数较治疗前和硝苯地平组均明显下降,具有显著性差异(P＜0.05).结论 替米沙坦除了具有强效、稳定降低血压的作用外,还具有改善IR胰岛β细胞功能、降低hs-CRP水平的作用.

研究证明许多心血管疾病如动脉粥样硬化(AS)、血管再狭窄、高血压、冠心病、脑血管疾病等的发生发展与一氧化氮合酶/一氧化氮(NOS/NO)的功能异常有着密切关系[1].因此,重建NOS/NO系统功能成为治疗心血管疾病的策略之一.

目的 探讨脑得生胶囊对家兔血管成形术后内皮功能和内膜增殖的影响.方法 雄性大耳白兔30只,随机分成4组:对照组(n=6),拉伤组(n=8),高脂组(n=8),脑得生组(n=8).采用高胆固醇喂养加腹主动脉内皮剥脱制作血管狭窄模型,之后行血管球囊扩张成形术.于术后4 w处死动物,取血管成形术部位血管标本,用免疫组化测定增殖细胞核抗原(PCNA)的表达水平.并分别于实验初、实验末兔耳缘静脉采血检测一氧化氮(NO)、内皮素(ET-1)浓度.结果 高脂组内膜增生最明显,内膜面积最大而管腔面积最小;脑得生组内膜面积较高脂组明显减小,管腔面积明显扩大.高脂组血清总胆固醇(TC)、低密度脂蛋白(LDL-C)和ET-1均明显升高,而血清NO明显下降;脑得生组血浆TC、LDL-C和ET-1明显降低,而血清NO水平明显升高.免疫组化染色:与高脂组比较,脑得生组PCNA的表达水平显著减少,有显著性差异(P＜0.05).结论 脑得生胶囊具有抑制家兔血管成形术后内膜增殖和保护血管内皮功能的作用.

目的 通过探讨兔腹主动脉成形术后血管再狭窄和MMP-2、TIMP1表达变化之间的关系,探讨脑得生胶囊预防再狭窄的可能机制.方法 健康雄性大耳白兔30只,随机分成对照组、拉伤组、高脂组、脑得生组.采用高胆固醇喂养加腹主动脉内皮剥脱制作血管狭窄模型,之后行血管球囊扩张成形术.于术后4 w处死动物,取血管成形术部位血管标本.进行光镜及免疫组化染色.结果 高脂组内膜增生最明显,内膜面积最大而管腔面积最小;脑得生组内膜面积较高脂组明显减小,管腔面积明显扩大.免疫组化染色:对照组无MMP-2和TIMP1表达,拉伤组只有微量表达.高脂组MMP-2和TIMP1表达明显升高,较对照组和拉伤组有显著差异(P＜0.05),经脑得生治疗后,MMP-2和TIMP1表达有下降趋势,MMP-2和TIMP1的比值较高脂组明显增大(P＜0.05).内膜的增生以及血管腔的狭窄程度与MMP-2和TIMP1的表达也有很好的相关性(r=0.54,P＜0.01).结论 脑得生胶囊可能足通过影响MMP-2和TIMP表达而抑制家兔血管成形术后的内膜增殖.

Objective To explore the relationship between C reactive protein(CRP) and left ventricular hypertrophy(LVH) and to examine whether angiotensin receptors antagonist ARB could decrease CRP expression,block or invert the progression of LVH with essential hypertension(EH).Methods 49 EH patients were divided into non-LVH group(n=23) and LVH group(n=26) by Devereux standard.All patients received telmisartan therapy for 24 w to detect blood pressure,hs-CRP and left ventricular mass index(LVMI).Results The hs-CRP level of LVH group was higher than that of non-LVH group.Hs-CRP was positively correlated with LVMI.Hs-CRP decreased obviously in non-LVH and LVH groups after treatment.LVMI decreased significantly than before treatment in LVH group(P<0.01).Conclusions Plasma CRP level is an independent risk factor for the development of LVH in EH.Telmisatan treatment can decrease the incident LVH by reducing CRP.

Objective To explore the inhibitory effect of Naodesheng capsule on the intimal proliferation and vascular remodeling after angioplasty in rabbits.Methods Thirty male whiter abbits were randomly divided into 3 groups: control group(n=6),injury group,high-lipid group,and Naodesheng group(n=8 in each group).The vascular structure model was established by peeling of the abdominal aortic endothelium with balloon and then performing abdominal aortic angioplasty.The rabbits were killed 4 weeks after angioplasty.The vessel samples from the site of angioplasty were examined by optical microscope and inununohistochemical staining.Results The results of optical microscopic examination showed that there were significant diferences in intimal area and luminal area between high-lipid group and naodesheng group.The results of inununohistochemical staining showed there was no expressing of MMP2 and TIMP1 in control group,low in injury group,high in high-lipid group.The expressing of MMP2 and TIMP1 in Naodesheng group had a significant decrease than those in high-lipid group.The intimal proliferation and the extent of narrow were related with MMP2 and TIMP1.Conclusions Naodesheng capsule can inhibit intimal proliferation and facilitate vascular remodeling after angioplasty.

Objective To study the neuroprotection of TAT-Flip in middle cerebral artery occlusion(MCAO)mice models.Methods 50 mice were divided into 5 groups:control,90 min MCAO,PBS MCAO and Flip MCAO and TAT-Flip MCAO groups to observe infarction volume and determine the protein expression of caspase 8,3 and Bcl-xl.Results TAT-Flip MCAO group had decreased infarction volume,the reduced protein expressions of caspase 8 and 3 and the increased Bcl-xl protein expression.Conclusions TAT-Flip could lessen brain injury,playing a neuroprotective role in MCAO mice models.

OBJECTIVE: To analyze the perspective and the key issue we have to be faced with in the gene therapy for treating hypertension. DATA SOURCES: An online search of Pubmed database was undertaken to identify relevant articles published in English between January 1996 and January 2006 by using the Keyword of "hypertension, gene therapy". Meanwhile, Chinese relevant literatures published between January 2000 and January 2006 were collected from Wanfang database, with the keywords of "hypertension, gene therapy" in Chinese. STUDY SELECTION: Inclusive criteria: Literatures were related to: ①the study of hypertension gene therapy strategies.②the study of the sense and antisense approach of gene therapy.③the study of vector for hypertension gene therapy. Exclusive criteria: Outdated or repetitive study and review. DATA EXTRACTION: Totally 195 relevant literatures with hypertension gene therapy were collected, and 14 of them were in accordance with the inclusive criteria. DATA SYNTHESIS: ①Two contrasting strategies have emerged for gene therapy in hypertension: The "knockdown" or gene expression reduction approach and the "overexpression" or gene induction approach. In the knockdown approach, genes are targeted to decrease their transcription and translation related to the pathophysiology of hypertension and angiocardiopathy. As for the overexpression approach, genes that are relevant in reducing high blood pressure are over expressed, thus increasing the substance benefit for vasodilatation.②In the gene therapy for hypertension, the vector, firstly should be able to transduce nondividing and slowly dividing cells with high efficiency. Secondly, the vector must possess sufficient capacity for the introduction of DNA, without any immunogenicity and toxic side effects. In addition, its integration site in the host genome must not cause disruption or mutation of other genes. Lastly, it should be easily produced in large scale.②The current problem we have to resolve in the gene therapy of hypertension includes the selection of target gene for hypertension and the construction of its vector. CONCLUSION: The most critical issue is the selection of target gene, the construction of the vector and the development of gene delivery system. Gene therapy can minimize the side effects associated with pharmacotherapy, cut down the morbidity of hypertension, and even cure hypertension.

Objective Through observing serum levels of true insulin,C peptide and blood glucose in the hypertension elderly to explore the relationship between hyperinsulinemia,insulin resistant(IR)and hypertension and the effect of telmisartan.Methods The fasting plasma glucose(FPG),true insulin,C peptide,blood fat,blood uric acid,IR index and islet β cell function index were determined in 20 non-obesity hypertension elderly(NHT group),15 obesity hypertension elderly(OHT group)and 20 healthy elderly(control group).The hypertension patients were given orally 80 mg telmisartan once a day to observe the changes of blood pressure and the above indexes 4 weeks later.Results The age,sex and FPG in three groups were matched.The serum levels of true insulin,C peptide and HOMA-IR and HOMA islet indexes in OHT and NHT groups were higher than those in control group.The blood pressue,true insulin,C peptide and HOMA-IR and HOMA islet indexes in hypertension patients after treatment with telmisartan were significantly lower than those before treatment(P<0.05).Conclusions IR,hyperinsulinemia and the increased compensative islet β cell function exsit in the elderly hypertension and nondiabetic patients,especially in those with obesity.Telmisartan could improve IR and islet β cell function,except effectively lower blood pressure.

目的应用蛋白质组学技术研究6-羟基多巴胺(6-OHDA)诱导PC12细胞帕金森病(PD)模型中钙结合蛋白1(CaBP1)的表达。方法在建立6-OHDA诱导PC12细胞帕金森病模型的基础上,分别提取6-OHDA处理组和对照组细胞总蛋白,应用荧光差异双向凝胶电泳(DIGE)技术获得蛋白点的差异表达信息,运用基质辅助激光解吸/电离飞行时间质谱仪(MALDI-TOFMS)鉴定出差异蛋白质。结果DIGE分析发现6-OHDA组表达明显增高的一个蛋白质点,经质谱分析鉴定确认为CaBP1。结论6-OHDA诱导PC12细胞的帕金森病模型中CaBP1表达增高,提示CaBP1增高可能与PD的发病机制有关。