β-Fg C448 G/A基因多态性、Fg水平与心肌梗死发生率的关系

目的:探讨β-Fg C 448 G/A基因多态性对血浆Fg水平的影响及其与心肌梗死(MI)发生率的关系.方法:应用多聚酶链反应-限制性片段长度多态性(PCR-RFLPs)的方法分析β-Fg C448 G/A基因多态性;比浊法测定血浆Fg水平.结果:75例MI患者(病例组)血浆Fg水平(3.73±1.08) g/L高于156例对照者(对照组)血浆Fg水平(3.08±0.71) g/L(P＜0.01).A448基因携带者血浆Fg水平高于GG基因型者(P＜0.05).病例组与对照组A448等位基因频率分别为0.313、0.276,二者比较有统计学意义(P＜0.01).结论:β-Fg C 448 G/A基因多态性与血浆Fg水平关联,A448基因携带者血浆Fg水平增高使MI易感性增加.     

Effects of atorvastatin on release of endothelial microparticles and myocardial apoptosis in rats with acute myocardial infarction

AIM: To investigate the effect of atorvastatin(AT) on the release of endothelial microparticles(EMP) and myocardial apoptosis in the rats with myocardial infarction. METHODS: SD male rats(n=24) were randomly divided into 3 groups:sham operation(sham) group, myocardial infarction(MI) group and MI+AT group. The rat model of acute myocardial infarction was prepared by coronary artery ligation. At 2 h and 24 h after modeling, the peripheral blood was collected to detect creatine kinase-MB(CK-MB) and cardiac troponin T(cTnT). The circulating levels of EMP were measured by flow cytometry. The myocardial apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) assay. RESULTS: At 2 h after modeling, the level of CK-MB was significantly increased in MI group compared with sham group, and the level of EMP and the myocardial apoptotic rate were significantly increased in MI group and MI+AT group compared with sham group. At 24 h after modeling, the level of EMP was significantly increased in MI group compared with sham group. The levels of CK-MB, cTnT, EMP and the myocardial apoptotic rate were significantly decreased in MI+AT group compared with MI group. Moreover, the level of CK-MB in MI group was significantly increased at 24 h compared with that at 2 h after modeling. The levels of CK-MB, cTnT and EMP were significantly decreased in MI+AT group at 24 h compared with those at 2 h after modeling. CONCLUSION: Ator-vastatin may reduce the level of EMP and the myocardial apoptotic rate in the rats with acute myocardial infarction, indicating that atorvastatin plays a role in protecting endothelium.     

MicroRNA profile analysis of ischemic myocardial tissues from rats with acute myocardial infarction

AIM：To identify differentially expressed microRNAs (miRNAs) in ischemic myocardial tissues from the rats with acute myocardial infarction (AMI) by miRNA array technique, and to predict their targets and analyze their functions using bioinformatics. METHODS：The rat models of AMI (n=3) were prepared by ligaturing the left anterior descending coronary artery (LAD) of Wistar rats. Electrocardiogram and blood pressure were detected during the operation, and the myocardial infarct size was measured by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining. Ischemic myocardial tissues were isolated from the infarct area 4 h after ischemia. The same procedure in sham group (n=3) was performed except for ligaturing LAD. Total RNA was extracted from ischemic and normal myocardial tissues. miRNA was isolated from total RNA, labeled with Cy3 and hybridized on miRNA array. Real-time PCR was applied to verify the reliability of miRNA array results. The targets of differentially expressed miRNAs were predicted and their functions were analyzed by bioinformatics. RESULTS：Rat model of AMI was successfully prepared and verified by electrocardiogram detection, blood pressure measurement and pathological observation. Compared with sham group, microarray screening showed that total 11 AMI-related miRNAs were selected, including 6 up-regulated and 5 down-regulated. Three of them (rno-miR-181c, rno-miR-146b and rno-miR-208) were related to the cardiovascular functions, while the functions of the others (rno-miR-672*, rno-miR-743b, rno-miR-128, rno-miR-138-1*, rno-miR-336, rno-miR-138-2*, rno-miR-325-3p and rno-miR-3572) were unknown and might be novel AMI-related biomarkers. Parts of the miRNA targets were also related to the cardiovascular functions. CONCLUSION：Differentially expressed miRNAs in AMI rats may serve as novel biomarkers for diagnosis of AMI and potential targets for treatment of AMI.     

三九舒血宁(银杏叶)注射液治疗急性脑梗死的临床观察

目的:观察三九舒血宁(银杏叶)注射液治疗急性脑梗死的疗效与安全性。方法:438例急性脑梗死患者随机分为治疗组(n=220)和对照组(n=218)。治疗组予生理盐水250mL 三九舒血宁(银杏叶)注射液12mL静脉滴注,1次/d,连用15d;对照组予低分子右旋糖酐注射液500mL 复方丹参注射液12mL静脉滴注,1次/d,连用15d。根据入院当日和治疗15d后神经功能缺损评分的减少、血液流变学及脑梗死灶的变化,并结合患者的生活能力进行评定疗效。结果:治疗组与对照组的临床疗效差异有统计学意义(H c=22.49,P<0.01);两组治疗前后的全血粘度、血浆粘度、红细胞聚集指数、甘油三酯、胆固醇、纤维蛋白原、脑梗死灶体积差异均有统计学意义(P<0.01),治疗后治疗组的指标优于对照组(P均<0.01)。治疗组无不良反应发生,对照组出现过敏性皮疹3例。结论:三九舒血宁(银杏叶)注射液治疗急性脑梗死疗效显著、安全。     

Effects of pretreatment with captopril on the infarct size and myocardial cell apoptosis in experimental rabbits

AIM:To investigate the effects of pretreatment of captopril on the infarct size and myocardial cell apoptosis in rabbits. METHODS:Rabbits were randomly divided into sham-operated control group (SO), acute infarct group (AI) and captopril pretreatment group (CP). The rabbits of CP group were treated with captopril (25 mg·kg^-1.d^-1) for 1 week before harvest. The left circumflex branch of coronary (LCX) was ligated to develop acute ischemic model. The systolic and diastolic function of left ventricle(LV) was measured before and at 15, 30, 60 min after ligating LCX, and the blood viscosity and hematocrit before and at 60 min after ligating LCX were measured also. 6 hours later LCX ligation, the hearts were harvested for determining the infarction size, which was expressed as the ratio of infarct area to the total ischemic area, and evaluating apoptosis index expressed as the percentage of myocardial cells with TUNEL positive staining. RESULTS:1.Compared with AI group, captopril pretreatment significantly reduced the infarction size (16.60%±0.94% vs 36.24%±1.94%, P＜0.05), and improved the LV function and viscosity of blood. 2. Apoptosis of myocardial cell was found in the myocardium surrounding to the infarction area, however, the apoptosis index of CP group was significantly lower than that of AI group (26.30%±0.71% vs 42.44%±2.32%,P＜0.05).CONCLUSION:Apoptosis of myocardial cell exists in the area surrounding the infarction. Captopril pretreatment can reduce infarction size and myocardial apoptosis index, and improve the LV function as well as blood viscosity in this acute ischemic model.     

Change of antithrombin Ⅲ in patients with atherosclerotic cerebral infarction

AIM：To explore the change of antithrombin Ⅲ (AT-Ⅲ) in the patients with atherosclerotic cerebral infarction. METHODS：Chromogenic substrate assay was used to measure the activity of AT-Ⅲ in 55 patients with atherosclerotic cerebral infarction and 55 healthy controls, and the correlation analysis was applied to determine the AT-Ⅲ activity with the severity of damage in central nervous system and general biochemical parameters. The levels of TNF-α and IL-6 in the plasma were detected by ELISA. Immunocomplex in the plasma was measured by enzyme immunoassay （EIA）. The number and phenotype of the monocytes in peripheral blood were analyzed by flow cytometry. ELISA was also applied to determine the secretion of TNF-α and IL-6 from the monocytes after the stimulation of immunocomplex. The expression of AT-Ⅲ in human brain vascular endothelial cells after the stimulation of TNF-α and IL-6 was observed by Western blotting. RESULTS：The activity of AT-Ⅲ significantly decreased in the patients with atherosclerotic cerebral infarction, and negatively correlated with the damage degree of nervous system function, systolic pressure, diastolic pressure, glucose, cholesterol, triglyceride, low-density lipoprotein cholesterol and homocysteine, while positively correlated with high-density lipoprotein. In addition, the plasma levels of TNF-α and IL-6 increased significantly, accompanied with the enhancement of immunocomplex level. The numbers of CD14+ CD16+ and CD14+ CD32+ monocytes in peripheral blood were not changed, while CD14+ CD64+ monocytes increased obviously. The secretion of TNF-α and IL-6 by monocytes were significantly enhanced after stimulated with immunocomplex, while the protein expression of AT-Ⅲ in the human brain vascular endothelial cells was down-regulated after co-incubated with TNF-α or IL-6. CONCLUSION：Decreased AT-Ⅲ activity in the patients with atherosclerotic cerebral infarction is one of the risk factors of cerebral infarction, and related with the disease severity. The production of pro-inflammatory cytokines through immunocomplex from CD14+ CD64+ monocytes may be involved in the mechanism. Improvement of AT-Ⅲ activity may protect against cerebral ischemia.     

白芍络石方治疗脑梗死后痉挛性瘫痪临床观察

目的 观察白芍络石方治疗脑梗死后痉挛性瘫痪的临床疗效及其安全性。方法 选取符合诊断的脑梗死后痉挛性瘫痪患者60例,采用随机、平行对照方法,分为中药组及对照组各30例。对照组予以常规治疗,中药组在常规治疗的基础上加用白芍络石方治疗,两组疗程均为4周。观察治疗前、治疗第2周末、第4周末的肌力（Robert Lovett法评定）、上肢肌张力（MAS评分评价）、下肢肌张力（CSS评分评价）、神经功能缺损程度（NIHSS评分评价）及日常生活能力（MBI评分评价）的变化,并观察干预后的不良反应。结果 治疗2周后中药组患者肢体上下肢肌力、上肢肌张力改善明显优于对照组（P<0.05）,治疗4周后中药组下肢肌力、MBI评分、NIHSS评分改善明显优于对照组（P<0.05）,且治疗过程中未出现明显血常规、肝肾功能异常等不良反应。结论 白芍络石方能改善脑梗死后偏瘫患者的运动能力,缓解偏瘫上肢的痉挛,提升其日常生活能力,且安全可靠。     

急性ST段抬高型心肌梗死紧急血运重建的临床疗效

目的探讨急性ST段抬高型心肌梗死（STEMI）紧急血运重建的临床疗效.方法 308例AMI患者分为紧急血运重建治疗组157例和药物治疗组151例.对所有患者随访4~88个月,平均随访（45±26）个月.观察住院期间和随访期间的心脏不良事件和超声心动图的变化,并利用QRS计分评估梗死范围的变化.结果 1）紧急血运重建组平均住院时间为（13.8±9.7）d,显著少于内科药物治疗组（19.8±8.9）d,P〈0.05;2）延迟血运重建组的复合终点事件发生率显著少于药物治疗组,P〈0.05,差异有统计学意义;3）随访期间,延迟血运重建组的心力衰竭及复合终点事件的发生率显著低于药物治疗组,P〈0.05;4）超声心动图随访结果示：紧急血运重建组的LVEF显著高于药物治疗组,差异有统计学意义,P〈0.05,紧急血运重建组的LVDd显著小于药物治疗组,P〈0.05;5）紧急血运重建组的心肌梗死范围回缩率（0.386±0.120）显著大于药物治疗组（0.273±0.096）,P〈0.05.结论紧急血运重建能减少住院期间和随访期间的心脏事件发生率,改善左室功能,使心肌梗死面积缩小,并改善AMI患者的预后.     

Effect of galectin-3 on ventricular remodeling in rabbits with ischemic cardiac insufficiency

AIM:To investigate the relationship between galectin-3(Gal-3) and myocardial fibrosis,and to clarify the role of Gal-3 in ventricular remodeling in rabbits with ischemic cardiac insufficiency.METHODS:A rabbit model of ischemic cardiac insufficiency was established by ligation of the anterior descending branch of the coronary artery.The 20 rabbits were randomly divided into sham operation group and cardiac insufficiency group by random number table method.After 4 weeks of coronary artery ligation,the cardiac function was measured by cardiac echocardiogram.Real-time PCR and Western blot were used to detect the expression of Gal-3,type I collagen and type Ⅲ collagen at mRNA and protein levels in the myocardium.The serum Gal-3 contents were measured by ELISA.HE staining and Masson staining were used to observe the degree of fibrosis development in myocardial tissues after infarction.RESULTS:Compared with sham operation group,the mRNA expression of Gal-3 in cardiac insufficiency group was significantly increased.At the same time,type I collagen,type Ⅲ collagen and collagen type I/Ⅲ ratio were also increased significantly.The protein contents of Gal-3,type I collagen and type Ⅲ collagen were increased significantly.The serum Gal-3 levels were significantly increased.The pathological changes were observed in cardiac insufficiency group as the myocardial cell morphological disorder and marked hyperplasia of fibrous tissue were seen.CONCLUSION:Gal-3 aggravates myocardial fibrosis in rabbits with ischemic cardiac insufficiency,and promotes the ventricular remodeling and the occurrence of heart failure.