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1.
目的探讨脑梗死患者血清基质金属蛋白酶9(MMP-9)和组织基质金属蛋白酶抑制剂1(TIMP-1)的动态变化及对临床预后的影响。方法选择急性脑梗死患者60例,按照TOAST分型方法将脑梗死患者分为3组,心源性脑栓塞(CE)组,大动脉粥样硬化性卒中(LAA)组,腔隙性脑梗死(SA)组,每组20例;另选健康体检者20例作为对照组,分别测定急性脑梗死患者发病24 h内,第5、10天的血清MMP-9、TIMP-1含量,记录患者入院时的美国国立卫生研究所脑卒中量表(NIHSS)评分;记录发病1、6个月时的Barthal指数(BI)来评价顸后。结果发病后24 h内,脑梗死各组患者血清MMP-9、TIMP-1含量较对照组均明显升高(P<0.05),其中,CE组和LAA组MMP-9、TIMP-1含量持续至第5天仍未下降.而SA组已逐渐降至正常水平。发病后24 h内血清MMP-9含量与相应时间段NIHSS评分呈正相关。近期预后较好患者发病24 h内血清MMP-9含量明显低于预后较差患者(P<0.05)。结论MMP-9与病情的严重程度有关。脑梗死后24 h内的血清MMIP-9含量是预后的独立预测因素。  相似文献   

2.
目的 评价药物与择期经皮冠状动脉介入治疗(PCI)对急性心肌梗死(AMI) 基质金属蛋白酶-1(MMP-1)及其抑制物-1(TIMP-1)的影响.方法 对2005年3月至2007年11月贵州省人民医院心内科的41例AMI患者在分别于强化内科药物(药物组,22例)和在此基础上行择期PCI介入(PCI组,19例)治疗.应用酶联免疫法检测AMI患者发病1周、3个月、6个月及12个月时的血清MMP-1和TIMP-1质量浓度.结果 与对照组比较,药物组与PCI组各组MMP-1均显著降低;除12个月外,各时点组TIMP-1均显著降低(P<0.05).两组组内比较,药物组12个月组TIMP-1较3个月及6个月组均显著升高(P<0.05).两组同期各时点组比较,PCI组3个月及6个月TIMP-1较同期药物组显著升高,同时其6个月组MMP-1/TIMP-1比值较同期药物组显著降低(P<0.05).结论 从抑制原有胶原网络降解的角度而言,择期PCI在AMI后6个月内明显优于药物治疗.而至12个月时择期PCI未进一步显示出此方面的优越性.  相似文献   

3.
目的研究骨髓间充质干细胞(BMSCs)移植对急性心肌梗死(AMI)后心功能不全家兔基质金属蛋白酶-9(MMP-9)、核转录因子-κB(NF-κB)表达的影响。方法以新西兰白兔为研究对象,随机分为对照组、AMI后心衰模型组、BMSCs移植组。采用开胸结扎冠状动脉前降支(LAD)的方法建立兔AMI后心功能不全动物模型,贴壁法分离、培养BMSCs,5-氮胞苷诱导、DAPI进行细胞标记。经透射电镜观察5-氮胞苷诱导的BMSCs。在AMI后14~21 d时,开胸移植自体BMSCs。超声心动图检查,观察心功能。采用ELISA检测血清MMP-9的浓度。实时荧光定量逆转录-聚合酶链反应(RT-PCR)的方法,于28 d检测心肌组织NF-кB、MMP-9 mRNA表达。结果①细胞移植后28 d,AMI后心衰模型组左室舒张未内径(EDD)明显超过正常对照组及BMSCs组,EF及FS均明显低于正常对照组及BMSCs组(P=0.005)。②手术后7 d,与正常对照组相比AMI后心衰模型组、BMSCs组的血清MMP-9的浓度均显著增加(P<0.05);细胞移植后28 d,BMSCs组的血清MMP-9的浓度比AMI后心衰模型组显著降低(P<0.05)。③BMSCs组心肌组织NF-κB、MMP-9 mRNA表达比AMI后心衰模型组显著降低(P<0.05)。④细胞移植后28 d时,EF与MMP-9呈负相关,与心肌NF-кB呈负相关。结论家兔自体BMSCs心肌移植可以抑制NF-κB活化,降低MMP-9mRNA表达,减轻左室重塑,改善AMI后心功能。  相似文献   

4.
目的:探讨急性心肌梗死(AMI)患者直接及择期经皮冠状动脉介入治疗(PCI)对左心室重构和左心功能的影响。方法:对42例初次发病、发病时间在12h以内或12~24h之间的AMI患者,行直接PCI;对30例AMI患者行择期PCI。于术后2、15和30周行二维超声心动图检查并记录有关心脏事件。结果:术后2、15周直接PCI组的左心室收缩末容积指数(ESVI)、左心室舒张末容积指数(EDVI)、左心室射血分数(LVEF)和梗死区室壁运动指数(RWMI)均显著优于择期PCI组(P<0.05或P<0.01)。择期PCI组、直接PCI组15和30周ESVI、EDVI、LVEF及RWMI与2周时比均有显著改善(P<0.05,P<0.01)。至30周时,直接PCI组和择期PCI组EDVI、LVEF和RWMI差异无统计学意义,而ESVI差异有统计学意义(P<0.05)。全心室壁运动指数在2组间始终差异无统计学意义(P>0.05)。结论:直接PCI及择期PCI均可有效抑制左心室重构和改善左心室功能,但直接PCI更优于择期PCI。  相似文献   

5.
目的研究COPD患者血清基质金属蛋白酶-9(MMP-9)抑制因子(TIMP-1)同细胞黏附因子-1(ICAM-1)、血管内皮黏附因子-1(VCAM-1)间的关系。方法 46例COPD患者和20例对照酶联免疫吸附法测量MMP-9,TIMP-1,ICAM-1及VCAM-1。结果 COPD组的MMP-9,TIMP-1,ICAM-1,VCAM-1显著高于对照组;MMP-9及TIMP-1均同ICAM-1,VCAM-1浓度呈正相关趋势(P<0.05);同时血清MMP-9,TIMP-1,ICAM-1,VCAM-1浓度同FEV1%,FEV1/FVC%呈负相关,MMP-9/TIMP-1比值同FEV1%,FEV1/FVC%呈负相关。结论 MMP-9,TIMP-1是造成COPD患者气流阻塞的重要因素。  相似文献   

6.
目的观察不同类型冠心病病人血清基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)、组织基质金属蛋白酶抑制物-1(tissue-inhibitor of metalloproteinase-1,TIMP-1)和血管紧张素Ⅱ(anginotensinⅡ, AngⅡ)的血清浓度及相关关系,探讨急性冠状动脉综合征发病机制。方法冠心病病人分为急性心肌梗死组、不稳定心绞痛组(上述两组合称急性冠状动脉综合征组)和稳定心绞痛组,每组病人30例,另设健康对照组30例,比较各组间血清MMP-9、TIMP-1、MMP-9/TIMP-1和AngⅡ水平。结果急性心肌梗死组和不稳定心绞痛组血清MMP-9、MMP-9/TIMP-1和AngⅡ水平高于对照组,差异有统计学意义(P<0.01),但稳定心绞痛组血清MMP-9、TIMP-1、MMP-9/TIMP-1和AngⅡ水平与对照组比较差异无统计学意义(P> 0.05),急性冠状动脉综合征组病人血清MMP-9、MMP-9/TIMP-1与AngⅡ水平呈正相关(P<0.01)。结论血清MMP-9、MMP-9/TIMP-1和AngⅡ水平的增高与急性冠状动脉综合征相关,可作为评价冠状动脉粥样硬化斑块稳定性与病变严重程度的一个参考指标。  相似文献   

7.
目的探讨基质金属蛋白酶9(mctalloprotemase-9,MMP-9)及组织基质金属蛋白酶抑制剂1(TIMP-1)与老年高血压患者颈动脉粥样硬化程度的相关性。方法选择老年高血压患者330例,应用高分辨超声测量颈动脉内膜中层厚度(IMT)及斑块情况,将患者分为4组:IMT正常组(26例)、IMT增厚组(80例)、稳定性斑块组(135例)和不稳定性斑块组(89例),测定血清生化指标、MMP-9、TIMP-1水平,进行组间比较。结果 IMT正常组、IMT增厚组、稳定性斑块组和不稳定性斑块组血清MMP-9、TIMP-1水平逐渐增高,不稳定性斑块组MMP-9/TIMP-1比值明显高于其他3组,差异有统计学意义(P<0.01)。取所有高血压患者进行多元线性逐步回归分析,颈动脉IMT与年龄、收缩压、LDL-C、空版(?)(?)相关(P<0.05,P<0.01);logistic回归分析显示,颈动脉是否存在斑块与体重指数、收缩压、LDL-C、logMMP-9相关(P<0.05,P<0.01)。取颈动脉斑块患者进行logistic回归分析,斑块是否稳定与收缩压、LDL-C、logMMP-9(模型1,P<0.05,P<0.01)或收缩压、LDL-C、logMMP-9/TIMP-1比值(模型2,P<0.05)相关。结论老年高血压患者血清MMP-9水平、MMP 9/TIMP-1比值与颈动脉是否存在斑块及其稳定性密切相关。  相似文献   

8.
目的 探讨单核细胞基质金属蛋白酶-9(MMP-9)及组织型基质金属蛋白酶抑制物-1(TIMP-1)mRNA表达与急性冠脉综合征(ACS)之间的关系.方法 分离8例ACS、8例稳定性心绞痛(SAP)及8例对照循环血单核细胞,采用异硫氰酸胍-酚-氯仿抽提法提取总RNA,扩增目的 基因MMP-9及TIMP-1 mRNA.根据冠脉造影进行冠脉狭窄程度计分并测定血清ox-LDL水平.结果 ①ACS患者外周血单核细胞MMP-9 mRNA表达与对照组比较增加(P<0.05),而TIMP-1 mRNA表达在各组间无差异;②ACS组血清ox-LDL浓度高于SAP组及对照组(P<0.05),且SAP组高于对照组(P<0.05),③单核细胞MMP-9 mRNA表达与血清ox-LDL浓度正相关(r=0.458,P=0.024);而与冠脉狭窄计分(CSS)无相关性.结论 ACS患者外周血单核细胞MMP-9、TIMP-1 mRNA表达比例失衡,可能直接参与了不稳定斑块的形成及破裂.  相似文献   

9.
目的探讨基质金属蛋白酶(MMP)-9和基质金属蛋白酶组织抑制因子(TIMP)-1在阿尔茨海默病(AD)模型大鼠脑海马CA1区的mRNA表达水平。方法将30只雄性Wistar大鼠,随机分为A、B、C、D、E组,每组6只。A组注射5μl生理盐水,B、C、D、E组双侧海马注射凝胶态Aβ25~355μl(依次含有Aβ25~350.5,1.0,5.0,10.0μg),大鼠于14 d后处死。取各组大鼠新鲜血清采用酶联免疫吸附试验(ELISA)检测肿瘤坏死因子(TNF)-α和白细胞介素(IL)-1β的表达量;取新鲜脑海马组织提取mRNA,qRTPCR技术检测MMP-9和TIMP-1 mRNA表达量。结果血清TNF-α含量D、E组明显高于A、B、C组(P<0.01);血清IL-1β含量D、E组明显高于A、B、C组(P<0.01)。MMP-9 mRNA表达量D、E组明显高于A、B、C组(P<0.01);TIMP-1 mRNA表达D、E组明显高于A、B、C组(P<0.01)。结论 Aβ所致AD大鼠脑内发生了炎症反应,MMP-9表达上调,而TIMP-1可与MMP-9特异性结合,进而抑制其活性,因此随着MMP-9上调,TIMP-1表达量也随之增加。  相似文献   

10.
目的观察罗格列酮(Ros)灌胃对兔急性心肌梗死(AMI)后心室重构的影响,并探讨其可能机制。方法将32只日本大耳白兔随机分为假手术(Sham)组、AMI模型组(AMI组)、Ros组、卡托普利(Cap)组,各8只。后3个组采用冠状动脉结扎法建立兔AMI模型。Ros组、Cap组分别予Ros 3 mg/(kg.d)和Cap 5 mg/(kg.d)灌胃,Sham组和AMI组予等量蒸馏水灌胃。4周后测量各组左室收缩末内经(LVESD)、左室舒张末内径(LVEDD)、左室射血分数(LVEF)、左室短轴缩短率(LVFS)和左室重量指数(LVMI),采用免疫组化检测各组心肌组织基质金属蛋白酶-9(MMP-9)及基质金属蛋白酶抑制剂-1(TIMP-1)。结果与Sham组比,AMI组LVESD、LVEDD、LVMI明显升高(P分别<0.01、0.01、0.05),LVEF、LVFS明显降低(P均<0.01),心肌组织中MMP-9/TIMP-1明显升高(P均<0.01);与AMI组比,Cap组和Ros组LVESD、LVEDD、LVMI明显减少(P分别<0.01、0.01、0.05),EF、FS明显升高(P均<0.01),心肌组织中MMP-9/TIMP-1明显降低(P<0.01);Ros与Cap组上述指标相近(P均>0.05)。结论 Ros灌胃可抑制兔AMI后心室重构、改善心功能,其可能是通过调节心肌组织中MMP-9/TIMP-1而发挥作用。  相似文献   

11.
目的:探讨急性冠状动脉综合征患者(ACS)外周血中脂联素与基质金属蛋白酶-9(MMP-9)及基质金属蛋白酶组织抑制因子-1(TIMP-1)水平及其相关性的研究。方法:急性心肌梗死组19例,不稳定性心绞痛组31例,稳定性心绞痛组13例,正常对照组22例,检测各组外周血中脂联素、MMP-9、TIMP-1的浓度。各组间采用独立样本的t检验,各参数之间进行单因素的相关分析。结果:急性心肌梗死组、不稳定性心绞痛组分别与正常对照组比较:外周血清中脂联素的浓度、TIMP-1的浓度均显著降低(P<0.05~0.01),MMP-9/TIMP-1及MMP-9的浓度则均显著升高(P<0.05~0.01);急性心肌梗死组、不稳定性心绞痛组与稳定性心绞痛组比较,脂联素的浓度显著降低(P<0.05~0.01),MMP-9/TIMP-1升高(P<0.05~0.01);稳定性心绞痛组与正常对照组比较各指标间无明显差异。相关性分析中:脂联素与MMP-9之间无相关性(r=-0.248,P>0.05),脂联素与TIMP-1有显著相关性(r=0.408,P<0.01),脂联素与MMP-9/TIMP-1之间有显著相关性(r=-0.478,P<0.001)。结论:ACS患者中,脂联素的分泌减少,导致TIMP-1的分泌也减少,MMP-9/TIMP-1平衡破坏,可能是急性冠状动脉综合征发生的重要因素。  相似文献   

12.
目的 检测慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)急性加重期、稳定期患者和健康对照者血清中基质金属蛋白酶-9 (matrix metalloproteinase-9,MMP-9)和组织型金属蛋白酶抑制物-1 (tissue inhibitor of met...  相似文献   

13.
谢立虎  陈战瑞  赵铖  黎艳  刘亚婧 《内科》2012,7(2):101-104
目的探讨系统性红斑狼疮(SLE)患者血清基质金属蛋白酶9(MMP-9)及其抑制物(TIMP-1)的表达特点及临床意义。方法用双抗体夹心酶联免疫吸附试验(ELISA)检测64例SLE患者(SLE组)和25名健康人(对照组)血清MMP-9和TIMP-1的水平并进行比较分析。结果 SLE组患者血清MMP-9水平明显低于对照组,TIMP-1明显高于对照组(P〈0.01),且MMP-9/TIMP-1低于对照组(P〈0.05);SLE患者活动期血清MMP-9、MMP-9/TIMP-1明显低于缓解期(P〈0.05),但TIMP-1的水平差异无统计学意义(P〉0.05);狼疮肾炎组MMP-9低于非肾炎组(P〈0.05),但TIMP-1差异无统计学意义(P〉0.05);MMP-9及TIMP-1水平在LN各病理类型患者中的差异无统计学意义(P〉0.05);患者的临床表现与MMP-9及TIMP-1水平无明显关系。结论 MMP-9及TIMP-1可能参与SLE的发病,血清MMP-9水平可作为反映SLE活动程度、肾脏损害的指标。  相似文献   

14.
Preventing left ventricular (LV) remodeling after coronary artery bypass graft surgery (CABG) is important to avoid long-term congestive heart failure. The present study evaluated the effects of angiotensin converting enzyme inhibitors (ACEIs) and beta-blockers on LV remodeling. Twenty-three patients with angina pectoris and 36 with old myocardial infarction underwent CABG. We assessed end diastolic volume index (EDVI), end systolic volume index (ESVI), and ejection fraction (EF) using left ventriculography before and after CABG. Changes in EDVI, ESVI, and EF were studied in the ACEI, beta-blocker, and control groups. Although EDVI was reduced in the ACEI group, ESVI and EF improved only slightly, whereas in the group given beta-blockers, ESVI was reduced, EF improved, and EDVI was minimally reduced. These results indicate that ACEIs and beta-blockers both protect against LV remodeling, although through different mechanisms.  相似文献   

15.
OSAHS、OSAHAHT最者血清基质金属蛋白酶9及其抑制因子水平   总被引:4,自引:0,他引:4  
目的 探讨阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)、阻塞性睡眠呼吸暂停低通气综合征相关性高血压(obstructive sleepapnea-hypopnea associated hypertension,OSAHAHT)患者血清基质金属蛋白酶9(MMP-9)及其抑制剂,基质金属蛋白酶组织抑制因子1(TIMP-1)水平的变化。方法 用酶联免疫吸附法对20例OSAHS、OSAHAHT患者血清MMP-9和TIMP-1水平测定,与16例健康对照组进行比较。结果 OSAHS、OSAHAHT患者血清MMP-9水平较正常对照组明显升高,有显著统计学意义,TIMP-1在OSAHS与对照组无明显差异,在OSAHAHT与对照组有明显差异,OSAHS、OSAHAHT患者血清MMP-9与反映睡眠呼吸暂停严重程度的指标有明显相关性。结论 OSAHS、OSAHAHT患者存在MMP-9及TIMP-1代谢的异常,血清MMP-9可反映睡眠呼吸暂停病情的严重程度。  相似文献   

16.
Ejection fraction (EF) and end-diastolic and end-systolic volume index (EDVI/ ESVI) derived from ventriculography are important prognostic parameters. Cine magnetic resonance imaging (MRI) using a steady-state, free-precession sequence (SSFP) offers excellent delineation of the endocardial borders and highly reproducible and accurate results for cardiac volumes. We evaluated MRI volumetry against routine x-ray ventriculography. In 200 patients EF, EDVI and ESVI were measured with MRI volumetry and x-ray ventriculography. The same MRI protocol was applied to 102 healthy persons in order to establish reference values. In healthy subjects mean EF was 68.8% +/- 5.4% (range 59-84%), mean EDVI 69 +/- 10 (43-90) and mean ESVI 22 +/- 5.8 (10-35 ml). In the patients, overall correlation (Spearman's R) of MRI with ventriculography was 0.86 for EF, 0.77 for EDVI and 0.88 for ESVI. For postextrasystolic beats (38% of the measurements), R was 0.73/0.65/0.73 for EF/EDVI/ESVI. MRI correlated best with biplane ventriculography during sinus rhythm (0.96/0.85/0.93); the worst correlation (0.78/0.81/0.83) resulted from patients with wall motion abnormalities in comparison to monoplane x-ray ventriculography. CONCLUSION: Contemporary MRI volumetry compares well to invasive data obtained under optimal conditions. In view of the known limitations of single plane ventriculography, MRI seems to allow exact volumetry independent from regional wall motion abnormalities.  相似文献   

17.
Antecedent hypertension adversely affects mortality and heart failure after myocardial infarction (MI). In addition, accelerated ventricular remodeling is a contributor to the increased mortality observed after MI. The purpose of this study was to assess the relationship of antecedent hypertension to ventricular remodeling after MI. Ninety-four patients presenting with a first acute MI who were treated with reperfusion therapy within 12 h of their symptom onset were enrolled in this study. All of them underwent left ventriculography immediately after reperfusion therapy and again at 6 months after the occurrence of MI. Patients were divided into two groups: a hypertensive group and a normotensive group. End-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) values in the acute phase were compared to those at 6 months after acute MI in either group. The hypertensive group showed a significant increase in both EDVI and ESVI after 6 months, whereas the normotensive group did not. In addition, there was no change in EF in the hypertensive group, whereas EF increased significantly after 6 months in the normotensive group. As a result, the percent changes in ESVI and EF were significantly different between the hypertensive group and normotensive group. The results demonstrated that antecedent hypertension interacts with ventricular cavity dilatation after MI.  相似文献   

18.
目的 探讨老年高血压患者颈动脉内膜中层厚度(IMT)与血清基质金属蛋白酶9(MMP-9)及基质金属蛋白酶组织型抑制剂1(TIMP-1)的相关性.方法 选择老年高血压患者135例作为高血压组,并按24 h动态脉压分为4个亚组,脉压≤40 mm Hg(1 mm Hg=0.133 kPa)为A组14例、41~60 mm Hg...  相似文献   

19.
BACKGROUND: Myocardial salvage has been shown to be dependent on the time elapsed from the onset of acute myocardial infarction (AMI) to reperfusion. The aim of this study was to evaluate the importance of time to reperfusion for left ventricular function recovery after primary angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) for AMI. METHODS: Ninety-five patients undergoing long-term successful PTCA for AMI were studied. Echocardiography was performed before and 3, 7, 30, 90, and 180 days after PTCA. End-diastolic volume index (EDVI) and end-systolic volume index (ESVI), ejection fraction, and left ventricular wall motion score index (WMSI) were evaluated. RESULTS: Patients were divided into group A, 23 patients reperfused within 2 hours; group B, 32 patients reperfused between 2 and 4 hours; group C, 22 patients reperfused between 4 and 6 hours; and group D, 18 patients reperfused between 6 and 12 hours. Both EDVI and ESVI were reduced in groups A and B at 90 days. Groups C and D did not show any changes of EDVI and ESVI at any stage throughout the study. Ejection fraction improved only in groups A and B at 30, 90, and 180 days. At study entry, WMSI was similar in all groups. After 7 days, in group A and in group B, WMSI was improved, no changes were observed in group C, and a mild deterioration was observed in group D at 3 and 7 days. Subsequent evaluations showed progressive improvement of WMSI in all groups. CONCLUSIONS: Myocardial salvage is achieved only in patients revascularized within 4 hours from AMI onset. However, revascularization after 6 hours may be worthwhile by preventing ventricular remodeling.  相似文献   

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