二氮嗪对异丙肾上腺素诱发的大鼠心肌缺血损伤的保护作用

目的 :评价线粒体三磷酸腺苷敏感性钾通道 (mitoKATP)开放剂二氮嗪 (diazoxide ,Diaz)对大鼠心肌缺血损伤的保护作用。　　方法 :选用Wistar大鼠 3 6只 ,分为对照组 8只、异丙肾上腺素 (ISO)组 10只、二氮嗪 10mg/kg组 9只和二氮嗪2 0mg/kg组 9只。用ISO 5mg/kg皮下注射复制大鼠心肌缺血损伤模型 ,2 4h后采血测定血清乳酸脱氢酶 (LDH)和肌酸激酶 (CK)活性及乳酸含量 ,同时监测心电图、血压和心率的变化 ,并观察心肌组织形态学改变。　　结果 :ISO引起大鼠心肌缺血损伤时 ,ISO组与对照组比较 ,血清LDH、CK活性和乳酸含量明显增加 ,有极显著性差异 (P <0 0 1) ,组织形态学也发生明显改变 ,心肌细胞损伤严重 ,有极显著性差异 (P <0 0 1)。预先口服二氮嗪 10～ 2 0mg/kg可逆转血清LDH、CK和乳酸的升高 ,有显著性差异 (P <0 0 5～ 0 0 1) ,减轻心肌细胞损伤程度。二氮嗪 10mg/kg不影响收缩压和心率。　　结论 :二氮嗪对ISO诱发的大鼠心肌缺血损伤具有保护作用     

线粒体ATP敏感性钾离子通道开放剂对冠心病大鼠血脂代谢和血管内皮损伤的影响及相关机制研究

背景线粒体ATP敏感性钾离子通道开放剂是一类扩血管药物,临床常用于治疗心脑血管疾病,但其对冠心病患者血脂代谢的影响、对血管内皮损伤的保护作用及相关机制尚不完全明确。目的探讨线粒体ATP敏感性钾离子通道开放剂对冠心病大鼠血脂代谢和血管内皮损伤的影响及机制。方法2018年8月-2019年2月,将50只6周龄SD大鼠随机分为对照组、模型组、低剂量组、中剂量组、高剂量组,每组10只。除对照组外,其他组大鼠均喂养高脂饲料、腹腔注射垂体后叶素制备冠心病大鼠模型,低、中、高剂量组大鼠分别按照二氮嗪3、5、7 mg/kg进行灌胃治疗,对照组、模型组大鼠均给予相同体积0.9%氯化钠溶液;五组大鼠均连续给药14 d。比较五组大鼠治疗前后血脂指标〔包括总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)〕,治疗后眼球血OD340值及颈动脉血管内皮细胞成纤维细胞生长因子2(FGF-2)、血管内皮生长因子(VEGF)相对表达量。结果治疗前模型组及低、中、高剂量组大鼠TC、TG、LDL-C水平高于对照组(P<0.05);治疗前五组大鼠HDL-C水平比较,差异无统计学意义(P>0.05);治疗后模型组及低、中、高剂量组大鼠TC、TG、LDL-C水平高于对照组,低、中、高剂量组大鼠TC、TG、LDL-C水平低于模型组,中、高剂量组大鼠TC、TG、LDL-C水平低于低剂量组,高剂量组大鼠TC、TG、LDL-C水平低于中剂量组(P<0.05);治疗后五组大鼠HDL-C水平比较,差异无统计学意义(P>0.05)。治疗后模型组大鼠眼球血OD340值低于对照组,中、高剂量组大鼠眼球血OD340值高于对照组,低、中、高剂量组大鼠眼球血OD340值高于模型组(P<0.05)。治疗后模型组及低、中剂量组大鼠颈动脉血管内皮细胞FGF-2及VEGF相对表达量高于对照组,低、中、高剂量组大鼠颈动脉血管内皮细胞FGF-2及VEGF相对表达量低于模型组(P<0.05)。结论线粒体ATP敏感性钾离子通道开放剂可通过抑制羟甲基戊二酰辅酶A(HMG-CoA)还原酶活性而改善冠心病大鼠血脂代谢,并可通过下调颈动脉血管内皮细胞FGF-2及VEGF的表达量而减轻血管内皮损伤。     

有氧运动联合抗阻力运动对糖尿病大鼠血管内皮功能的作用及其对磷脂酰肌醇-3激酶/蛋白激酶B/内皮型一氧化氮合酶通路的影响

目的探讨有氧运动联合抗阻力运动对糖尿病大鼠血管内皮功能及对磷脂酰肌醇-3激酶/蛋白激酶B/一氧化氮合酶(PI3K/Akt/eNOS)通路的影响。方法将SD大鼠随机分为对照组(NC)、糖尿病模型组(DM)、单纯有氧运动训练组(AE)、单纯抗阻力运动训练组(RE)及有氧运动+抗阻力运动训练组(ARE),检测各组内皮功能指标、PI3K/Akt/eNOS通路基因及蛋白表达情况。结果乙酰胆碱(Ach)浓度在3×10~(-5) mol/L时,ARE组舒张率高于AE组和RE组(P0.05)。ARE组VEGF、一氧化氮(NO)表达量高于DM组[(21.45±3.48)vs(8.23±1.14)pg/ml,(25.67±3.19)vs(8.89±1.56)μmol/L,P0.05]。ARE组PI3K、Akt及eNOS基因相对表达量高于DM组[(4.08±0.83)vs(0.27±0.11),(2.75±0.69)vs(0.26±0.09),(4.25±0.74)vs(0.59±0.19),P0.05]。ARE组PI3K、磷酸化Akt(p-Akt)及磷酸化eNOS(p-eNOS)蛋白相对表达量高于DM组[(0.78±0.21)vs(0.20±0.09),(1.21±0.38)vs(0.54±0.19),(0.59±0.23)vs(0.16±0.08),P0.05]。结论有氧运动联合抗阻力运动能改善糖尿病大鼠血管舒张功能,促进VEGF、NO的释放,作用与激活PI3K/Akt/eNOS信号通路有关。     

加速康复外科理念在老年患者行腹腔镜胆道探查术中的应用

目的探讨加速康复外科(ERAS)理念下行腹腔镜胆道探查术(LCBDE)对老年胆总管结石患者的效果。方法入选2014年2月至2018年3月内蒙古医科大学第三附属医院普外科收治的老年胆总管结石患者120例,随机数字表法分为ERAS组及对照组,每组60例。ERAS组给予加速康复方案治疗,对照组给予常规治疗,比较2组患者的术后疗效、术后并发症及术后镇痛效果。采用SPSS 18. 0统计软件对数据进行处理。组间比较采用t检验、χ~2检验或秩和检验。结果 ERAS组患者相比对照组患者术后下床时间[(9. 62±2. 35) vs (22. 51±3. 32) h]、排气时间[(22. 13±5. 12) vs(37. 51±6. 43)h]、进食时间[(18. 75±3. 28) vs (34. 69±4. 47)h]、住院天数[(9. 73±1. 48) vs (14. 73±2. 92)d]明显提前,住院费用降低[(1. 68±0. 23)×10~4vs (2. 47±0. 32)×104RMB$],肺部感染[5. 00%(3/60) vs 13. 33%(8/60)]、尿路感染[3. 33%(2/60) vs 11. 67%(7/60)]、腹胀发生率[8. 33%(5/60) vs 20. 00%(12/60)]均降低,差异均具有统计学意义(P 0. 05)。ERAS组患者术后镇痛达到优者占81. 67%(49/60),明显高于对照组的48. 33%(29/60),差异有统计学意义(P 0. 05)。结论老年患者在ERAS原则下行LCBDE安全、有效,值得推广。     

枸杞多糖通过调节热休克蛋白B8介导的自噬改善糖尿病神经病理性疼痛的研究

目的探讨枸杞多糖(LBP)通过调节热休克蛋白B8(HSPB8)介导的自噬改善糖尿病神经病理性疼痛(DNP)及其作用机制。方法 62只SD大鼠随机选取10只为正常对照组(NC),其余腹腔注射STZ建立糖尿病大鼠模型,随机分为糖尿病组(DM)、LBP组、α-硫辛酸组(LA),每组各15只。每4周检测各组大鼠的机械缩足反射阈值(PWT)和热缩足反射潜伏期(PWL)。治疗12周后,采用Western blot、免疫组织化学法检测腰段脊髓神经中HSPB8、Bcl-2相关永生化基因3(BAG3)、微管相关蛋白轻链3-Ⅱ(LC3-Ⅱ)、P62蛋白表达量。结果与NC组比较,DM组在4、8、12周时PWT、PWL降低(P0. 05或P0. 01)。与DM组比较,LBP组在4、8、12周时PWT、PWL升高(P0. 05或P0. 01)。Western blot法检测显示,与NC组比较,DM组HSPB8、BAG3、LC3-Ⅱ蛋白表达量降低[(0. 17±0. 04)vs(0. 13±0. 04)、(0. 35±0. 11)vs(0. 14±0. 04)、(0. 31±0. 03)vs(0. 17±0. 05),P0. 05或P0. 01],P62蛋白表达量升高[(0. 37±0. 03)vs(0. 63±0. 08),P0. 01)]。与DM组比较,LBP组HSPB8、BAG3、LC3-Ⅱ蛋白表达量升高[(0. 13±0. 04)vs(0. 21±0. 03)、(0. 14±0. 04)vs(0. 32±0. 09)、(0. 17±0. 05)vs(0. 34±0. 08),P0. 01],P62蛋白表达量降低[(0. 63±0. 08)vs(0. 39±0. 14),P0. 01)]。免疫组织化学法检测显示,与NC组比较,DM组HSPB8、BAG3、LC3-Ⅱ蛋白表达量降低[(168. 24±10. 21)vs(144. 83±14. 53)、(146. 50±13. 48)vs(124. 83±9. 33)、(144. 33±7. 77)vs(127. 83±5. 92),P0. 01],P62蛋白表达量升高[(146. 67±14. 10)vs(175. 83±9. 22),P0. 01)]。与DM组比较,LBP组HSPB8、BAG3、LC3-Ⅱ蛋白表达量升高[(144. 83±14. 53)vs(180. 0±7. 95)、(124. 83±9. 33)vs(155. 0±5. 76)、(127. 83±5. 92)vs(156. 32±5. 56),P0. 01],P62蛋白表达量降低[(175. 83±9. 22)vs(139. 67±12. 68),P0. 01)]。结论 LBP可能通过提高糖尿病大鼠脊髓神经中HSPB8促进自噬缓解DNP。     

内脂素基因过表达对大鼠胰岛素敏感性和血浆FGF-21水平的影响

目的 探讨内脂素基因过表达对大鼠胰岛素敏感性和血浆成纤维细胞生长因子21(FGF-21)的影响.方法 构建大鼠内脂素基因重组真核表达质粒,将该质粒转染大鼠.在转染前后采用正糖-高胰岛素钳夹技术评价大鼠胰岛素敏感性变化,并采用放射免疫法测定其血浆FGF-21浓度.结果 在质粒注射后3 d大鼠血清内脂素水平明显升高(1.49±0.06 vs 0.99±0.04,P<0.01);葡萄糖输注率(GIR)[(35.3±1.4 vs 27.6±1.7)mg·kg-1·min-1,P<0.01]较注射前明显升高;基础血浆胰岛素水平明显下降[(14.5±3.7 vs 24.4±6.2)mU/L,P<0.05];总胆固醇、高密度脂蛋白胆固醇明显降低[(1.31±0.10 vs1.76±0.22)mmol/L和(0.59±0.04 vs 0.95±0.15)mmol/L,均P<0.05];血浆FGF-21也降低[(2.25±0.19 vs 2.59±0.23) μg/L,P<0.05];在转染前后基础血糖和血浆脂联素水平无明显变化.结论 内脂素质粒转染使大鼠血浆vsfatin水平升高和FGF-21水平降低,胰岛素敏感性增强.     

心肌线粒体三磷酸腺苷敏感性钾通道开放剂二氮嗪对体外大鼠心肌缺血再灌注损伤的影响

近年来研究证明 ,心肌线粒体ATP敏感性钾通道(mitoKATP)是心肌缺血的重要治疗靶点[1 ] 。 2 0世纪 6 0年代二氮嗪作为抗高血压药在美国合成并上市 ,近来研究表明 ,二氮嗪是mitoKATP开放剂 ,具有耐缺血缺氧损伤的心脏保护作用。本研究采用体外大鼠心肌缺血再灌注损伤模型 ,观察了二氮嗪对冠状动脉流量、灌流液乳酸脱氢酶 (LDH)活性等的影响。1　材料与方法大鼠断颈后迅速取下心脏 ,置于预先充氧的K H缓冲液中 ,行主动脉根部逆行插管 ,悬挂于Langendroff装置上 ,灌注含有 95 %O2 和 5 %CO2 的K H缓冲液 (pH 7.4 ,37℃ )。平衡灌注 1…     

原发性血小板增多症伴随轻度骨髓网状纤维增多患者的危险因素

目的:探索伴随骨髓网状纤维增多原发性血小板增多症(essential thrombocythemia, ET)患者的危险因素。方法:将58例ET患者根据是否伴有轻度骨髓网状纤维增多(1级)分为增多组(29例)和无增多组(29例),比较2组患者间基线资料、基因突变、血常规、生化、骨髓细胞学、骨髓活检等指标差异，进一步多因素回归分析影响ET患者伴随轻度骨髓网状纤维增多的独立危险因素。结果:与无增多组比较，增多组患者的TET2突变频率(30.77%vs 8.33%,P=0.048)、血小板计数(PLT)[(820.93±242.95)×10⁹/L vs (673.93±174.00)×10⁹/L,P=0.01]、乳酸脱氢酶[(285.63±97.60) U/L vs(213.46±45.14) U/L,P=0.02]、造血容量[(62.00±15.75)%vs (53.20±12.82)%,P=0.04]、粒系细胞占比[(63.64±8.61)%vs (57.70±8.80)%,P=0.02]、粒红细胞比[(4.01±2.02) vs (2.88±...     

阿托伐他汀对糖尿病心肌梗死大鼠视网膜及心肌血管新生双向性研究

目的探讨阿托伐他汀对糖尿病心肌梗死大鼠视网膜心肌血管新生的双向性作用及机制。方法雄性SD大鼠80只,随机分为3组。正常组30只,心梗组(AMI组)25只,糖尿病心梗组(AMI+DM组)25只。通过结扎前降支建立心肌梗死模型,腹腔注射链脲佐菌素65 mg/kg建立糖尿病模型。糖尿病心肌梗死模型以结扎前降支先建立心肌梗死模型再腹腔注射脲佐菌素建立糖尿病模型,造模成功后,开始以2.5 mg/250 g剂量阿托伐他汀溶液灌胃,正常组以同等剂量生理盐水灌胃,大鼠分别于4个月时按比例随机处死。取心脏、视网膜做免疫组化观察心肌组织、视网膜血管内皮生长因子(VEGF)蛋白的表达情况。结果 AMI组心肌细胞VEGF表达高于正常组心肌细胞VEGF表达[(7158.4±525.2) vs.(3263.5±454.5)ng/L],AMI+DM组VEGF表达也高于正常组[(7058.4±435.7) vs.(3263.5±454.5)ng/L],差异均有统计学意义(P0.05);AMI+DM组视网膜VEGF表达低于正常组VEGF表达[(2671.2±424.1)vs.(3345.5±321.5)ng/L],也低于AMI组[(2671.2±424.1)vs.(3097.5±310.7)ng/L],差异均有统计学意义(P0.05)。结论他汀类药物能够在促进心肌梗死心肌VEGF蛋白表达的同时抑制糖尿病大鼠视网膜VEGF表达,在延缓视网膜病变进展的同时促进梗死心肌部位血管新生。     

线粒体KATP开放剂二氮嗪对家兔心肌缺血—再灌注损伤的影响

目的 观察线粒体ATP敏感性钾通道(KATP)开放剂二氮嗪对家兔心肌缺血—再灌注(I/R)损伤的影响.方法 将家兔随机分为A、B、C、D组各8只,分别于造模前30 min经耳缘静脉给予二氮嗪溶剂及1、3、5 mg/kg的二氮嗪;结扎家兔左冠状动脉前降支,进行30 min缺血和120 min的再灌注,建立心肌I/R损伤模型.在缺血和再灌注期,监测家兔的血压、心率、心电图和血清肌酸激酶(CK)的变化,用计算机图像分析测定心肌梗死面积.结果 与A组比较,B、C组对家兔血压和心率无明显影响,D组可明显降低血压(P＜0.01).A组心肌梗死面积占左心室总面积的百分比为22.7％±9.2％,B、C、D组分别为19.1％±5.8％、12.7％±4.5％、11.8％±7.2％;与A组比较,C、D组梗死面积分别下降了44.1％、48.0％(P均＜0.05).与A组比较,C组CK于再灌注1、2h分别下降16.3％、25.8％,D组分别下降31.8％、45.6％(P均＜0.01).结论 线粒体KATP开放剂二氮嗪对家兔心肌I/R损伤具有保护作用.     

血管内皮生长因子与冠状动脉粥样硬化及侧枝循环形成的关系

探讨血管内皮生长因子与冠状动脉粥样硬化狭窄程度及冠状动脉侧枝循环形成的关系 ,应用酶联免疫吸附法检测 10 2例经冠状动脉造影确诊的冠心病患者和 43例冠状动脉造影正常者的冠状动脉血浆血管内皮生长因子浓度 ,作冠状动脉病变Leaman记分和侧枝循环Rentrop分级 ,并分析血管内皮生长因子与其的关系。结果发现 ,冠心病患者冠状动脉血浆血管内皮生长因子平均浓度明显高于正常对照组 ( 2 2 5± 147ng L比 74± 5 2ng L ,P <0 .0 1) ,而且冠心病患者中侧枝循环形成者血管内皮生长因子平均浓度明显高于无侧枝循环形成者 ( 2 99± 15 2ng L比 2 0 2± 12 2ng L ,P <0 .0 5 ) ;血浆血管内皮生长因子浓度与Leaman记分呈显著正相关 (r=0 .693 ,P <0 .0 0 1)。结果提示 ,血管内皮生长因子与冠状动脉粥样硬化狭窄程度及冠状动脉侧枝循环形成具有一定的关系 ,血管内皮生长因子可能既有促进冠状动脉侧枝循环形成的作用 ,又在动脉粥样硬化发展中起到一定的双重调节作用     

Critical timing of mitochondrial K(ATP) channel opening for enhancement of myocardial tolerance against infarction

Objective The present study was designed to assess the relationship between the timing of a mitoK_ATP channel opener, diazoxide, and its infarct size-limiting effect. Methods In isolated rabbit hearts, infarction was induced by 30 min of global ischemia and 2 h of reperfusion, and infarct size was determined by tetrazolium staining and expressed as a percentage of the left ventricle (%IS/LV). Diazoxide, a mitoK_ATP channel selective opener, and/or 5-hydroxydecanoate (5-HD), a mitoKATP channel blocker, were infused before or after the onset of ischemia. When these agents were infused during the ischemic period, they were dissolved in a hypoxic buffer at concentrations 10-fold higher than those in the pre-ischemic period, and the infusion rate was set at 2 % of the pre-ischemic coronary flow. Results In untreated controls, %IS/LV was 53.2 ± 4.1 (SE). Pretreatment with diazoxide (100 μM) with a 10-min washout period reduced %IS/LV to 7.8 ± 2.4 and this protection was abolished by co-infusion of 5-HD (50 μM). Pre-ischemic infusion of diazoxide without a washout period reduced %IS/LV to 7.3 ± 1.4, and infusion of diazoxide from 10 min after the onset of ischemia also limited %IS/LV to 14.9 ± 4.6. However, diazoxide infusion from 25 min after the onset of ischemia failed to reduce infarct size (%IS/LV = 54.5 ± 7.2). Furthermore, pretreatment with 5-HD (50 μM) also completely abolished the protection afforded by early post-ischemic diazoxide infusion (%IS/LV = 48.3 ± 6.5). Neither infusion of 5-HD nor the anoxic vehicle alone during ischemia modified %IS/LV. Conclusion These findings suggest that opening of mitoK_ATP channels before ischemia and during early ischemia, but not that upon reperfusion, is important for enhancement of myocardial tolerance against infarction. Received: 6 November 2000, Returned for revision: 21 November 2000, Revision received: 24 January 2001, Accepted: 25 January 2001     

The myocardial oxygen supply/demand ratio in patients with and without coronary artery disease

This study was performed to assess the relationship between coronary sinus blood flow (by thermodilution) and myocardial oxygen demand (heart rate-systolic arterial pressure double product) during atrial pacing in patients with and without coronary artery disease. In 11 individuals with coronary artery disease, pacing was performed to ischemia, as reflected by electrocardiographic changes or lactate production; 8 patients without coronary artery disease served as controls. Coronary sinus blood flow (in ml/min) was similar for the two groups at rest. However, the increase in coronary blood flow from rest to peak pacing was less (P = 0.025) in those with coronary artery disease (50 ± 26 ml/min) than in controls (79 ± 26 ml/min). The ratio of coronary sinus blood flow to double product was the same at rest in both groups (11.1 ± 2.2 × 10^?3 controls, 11.6 ± 2.7 × 10^?3 coronary artery disease; NS). At peak pacing, it was unchanged in the controls (10.4 ± 2.0 × 10^?3) but fell in those with coronary artery disease (9.0 ± 2.5 × 10^?3; P = 0.002). The aortic-coronary sinus oxygen content difference was similar at rest in both groups and did not change in response to pacing in either group. Thus, in response to augmented myocardial oxygen demand, patients without coronary artery disease have an appropriate increase in coronary blood flow and myocardial oxygen supply, while in those with coronary artery disease who develop ischemia the increment in myocardial blood flow (and oxygen supply) is inappropriately low.     

Long-term clinical outcomes in patients treated with drug-eluting compared to bare-metal stents for the treatment of transplant coronary artery disease

Objective : We aimed to compare the long‐term clinical outcomes of first‐vessel percutaneous coronary intervention (PCI) with drug‐eluting stents (DES) and bare metal stents (BMS) for the treatment of transplant coronary artery disease (TCAD). Background : TCAD is the leading cause of late death in orthotopic heart transplantation (OHT) recipients. PCI is associated with worse clinical outcomes compared with non‐OHT patients. Our institution previously reported superior angiographic outcomes with DES compared with BMS in OHT patients. However, long‐term clinical outcomes comparing PCI with DES versus BMS are lacking. Methods : The data on 105 OHT recipients who underwent first‐vessel PCI with DES (n = 58) or BMS (n = 47) at UCLA Medical Center between 1995 and 2009 were retrospectively analyzed. Results : Five‐year clinical outcomes were not significantly different with DES and BMS in terms of the composite of death, myocardial infarction (MI), or target vessel revascularization (TVR) [(40.8 ± 7.2)% vs. (59.6 ± 7.2)%, log‐rank P = 0.33], death [(31.8 ± 7.8)% vs. (40.4 ± 7.2)%, log‐rank P = 0.46], MI [(12.2 ± 6.2)% vs. (11.3 ± 5.4)%, log rank P = 0.98], TVR [(25.5 ± 6.9)% vs. (26.5 ± 7.3)%, log rank P = 0.76], and time to repeat OHT [(2.27 ± 1.79) vs. (3.22 ± 3.34), P = 0.98]. Conclusions : At long‐term follow‐up, PCI with DES and BMS provided similar clinical outcomes in OHT. Long‐term mortality remains high in OHT recipients after PCI with either DES or BMS. Randomized clinical trials are required to determine the optimal treatment strategy for OHT recipients with TCAD. © 2012 Wiley Periodicals, Inc.     

奥拉西坦对心肌缺血/再灌注损伤的保护作用

目的 研究奥拉西坦对心肌缺血/再灌注损伤(MI/RI)的保护作用及其机制。方法 32只大鼠依据随机数表法分为4组,每组8只:(1)假手术组;(2)MI/RI组;(3)低剂量组(奥拉西坦30mg/kg);(4)高剂量组(奥拉西坦50mg/kg)。低剂量组和高剂量组的16只大鼠手术前除正常饲养外,通过灌胃方式给予对应剂量的奥拉西坦,1次/d,连续7d。结扎大鼠冠状动脉前降支,建立MI/RI模型。酶联免疫吸附测定大鼠血清中肌酸激酶同工酶MB(CK-MB)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、白细胞介素-6(IL-6)和丙二醛(MDA)。测定心肌梗死面积百分比、心肌细胞凋亡率和Bcl-2/Bax比值。采用SPSS 21.0软件进行统计分析。组间比较采用单因素方差分析。结果 与MI/RI组比较,低剂量组和高剂量组大鼠的心肌梗死面积百分比(36.2%和13.6%和22.3%)、心肌细胞凋亡率(45.4%和30.6%和21.3%)、血清中CK-MB[(97.50±8.54)和(75.24±5.62)和(63.10±7.23)U/L]、LDH[(900.02±57.74)和(660.62±49.84)和(577.37±54.09)U/L]、MDA[(88.84±3.26)和(66.47±6.25)和(57.08±4.99)U/L]和IL-6[(186.39±10.18)和(153.34±6.81)和(143.31±9.08)pg/ml]含量均显著降低(P<0.05),而SOD[(15.22±1.24)和(24.80±3.32)和(34.82±3.66)U/ml]和Bcl-2/Bax比值(0.19和0.47和1.16)显著增加(P<0.05)。结论 奥拉西坦可能通过减轻氧化应激反应来抑制线粒体途径的细胞凋亡来保护MI/RI的心肌。     

p53信号通路在半枝莲总黄酮预处理大鼠心肌缺血再灌注损伤中的作用

目的 探讨半枝莲总黄酮(SBF)对心肌缺血/再灌注损伤(MI/RI)模型的保护作用及相关机制.方法 将50只SD雌性大鼠按照随机数表法随机分为5组,每组10只:(1)假手术组;(2)MI/RI组;(3)低剂量组(SBF 30mg/kg);(4)中剂量组(SBF 75mg/kg);(5)高剂量组(SBF 140mg/kg...     

老年心房颤动患者的冠状动脉病变分析

目的观察老年患者心房颤动(房颤)的发生与冠心病的关系。方法根据我院1990年以来的尸检资料,选择75岁以上生前有房颤发作记录的76例患者作为房颤组,平均年龄(86.9±6.9)岁,临床均诊断有冠心病;选择与房颤组年龄相近、临床无房颤记录、经尸检病理证实为冠心病的85例患者作为冠心病组,比较两组患者冠状动脉的病变情况。结果房颤组中38例患者经病理证实有冠心病,心肌梗死发生率为39.5%,冠心病组心肌梗死发生率为62.4%,两组比较有统计学差异(P<0.01);房颤组与冠心病组心脏重量、左心室壁厚度分别为[(437.5±80.6)%(434.6±90.3)g,P>0.05;(1.42±0.33)%(1.42±0.38)cm,P>0.05];房颤组冠状动脉达Ⅲ级病变和Ⅳ级病变的血管数量(40 vs.99、27 vs.52,P<0.001)明显少于冠心病组。结论老年患者心房颤动的发生与冠心病之间不存在明确的因果关系。     

Coronary hemodynamic data in ischemic heart disease according to ischemic behavior during pacing

In order to study the circulatory changes induced by maximal atrial pacing in coronary patients, coronary sinus blood flow (CBF) measured by continuous thermodilution, lactate extraction coefficient (K), arteriovenous difference in oxygen (AVO₂ diff), and aortic blood pressure (BP) were measured at basal state and at maximal heart rate (HR_max) in 11 patients without coronary disease (group I) and in 28 patients with severe coronary lesions, divided into two groups according to the absence (group IIa) or the presence (group IIb) of chest pain and ST-segment depression at HR_max. K was inverted in group IIb (24±17% vs −23±39%, p < 0.001), but remained unchanged in group I and group IIa. Despite similar HR_max, percent increase in CBF was significantly lower in group IIb (54±34%), than in group I (113±54%, p < 0.01). This contrasts with the higher values of the product of heart rate times systolic blood pressure (HR × SBP) as well as of diastolic blood pressure (DBP) in group IIb. The decrease in coronary resistances was lower in group IIb than in group I (p < 0.001), and also lower than in group IIa (p < 0.05). The ratio MO₂ × CBF/systolic BP × HR_max was significantly lowered only in group IIb (p < 0.001) confirming the imbalance between myocardial oxygen supply and oxygen demand. In coronary patients, myocardial ischemia induced by atrial pacing is related to an insufficient increase in CBF, well evidenced by continuous thermodilution.     

黄芪甲苷Ⅳ对梗死小鼠心肌新生血管成熟及HIF-1α、VEGF蛋白表达的影响

目的 观察黄芪甲苷（Astragaloside,Astra）-Ⅳ对梗死小鼠心肌新生血管成熟及缺氧诱导因子（Hypoxia induced factor,HIF）-1α和血管内皮生长因子（Vascular endothelial cell factor,VEGF）蛋白表达的影响。 方法 结扎法制备小鼠心肌梗死（Myocardium Infarct,MI）模型,Astra-Ⅳ腹腔注射[2 mg/（kg·d）]21 d,通过小动物超声系统评价小鼠心功能;计算梗死面积（IS）与缺血区面积（AAR）的比值;CD31和α-SMA双荧光染色法观察梗死周边心肌组织新生和成熟血管密度;经鼠尾注射FITC-Lectin观察新生血管的灌注情况;Western blot检测MI区及其边缘组织HIF-1α、VEGF表达的变化。 结果 Astra-Ⅳ可提高小鼠的FS（%）和EF（%）[（61.0±2.7）% vs.（40.2±3.9）%,P<0.05;（44.1±3.2）% vs.（29.1±4.1）%,P<0.05],减少MI范围[28.8±8.4）% vs.（45.1±9.3）%;P<0.05];MI+Astra-Ⅳ组心肌新生血管密度（214.0±21.3/mm2）,成熟血管密度（7.0±2.1/mm2）,有效灌注新生血管密度为（0.39±0.11）×105/pixels,与MI组比较均具有显著差异（P<0.01）;MI+Astra-Ⅳ组显著增加周围组织的HIF-1α、VEGF蛋白水平（P<0.01）。 结论 Astra-Ⅳ缩小MI面积,提高梗死心肌功能,并促进促血管新生和成熟,实现缺血组织有效灌注,其分子机制可能与HIF-1α和VEGF蛋白的表达增加有关。     

Importance of α1-sympathetic activity for diurnal change in ischemic threshold in patients with stable angina

Background: Although ischemic threshold reportedly is lower in the early morning than in the afternoon, the mechanisms that account for the diurnal change in minimal coronary vascular resistance in the potentially ischemic area are unknown. Hypothesis: We hypothesized that calcium-channel blockers and α₁ blockers may affect the ischemic threshold in the early morning and afternoon in patients with stable angina. Methods: Before and after the administration of the calcium antagonist amlodipine (5 mg) alone and combined with the α₁ blocker prazosin (1 mg), a treadmill exercise test using the Balke-Ware protocol was undertaken in the morning (8:00 A.M.) and repeated in the afternoon (1:00 P.M.) with 15 stable angina patients. The ischemic threshold was defined as a reciprocal of minimal coronary vascular resistance in the presence of comparable levels of myocardial ischemia indicated by 0.1 mV ST depression. Minimal coronary vascular resistance was calculated as mean blood pressure divided by coronary blood flow. Since the coronary blood flow is closely related to myocardial oxygen consumption, which can be replaced by the double product of heart rate and systolic blood pressure, minimal coronary vascular resistance was approximated to 1/heart rate. Results: At baseline, minimal coronary vascular resistance was significantly higher in the early morning than in the afternoon (8.5 ± 0.3×10^?3 min/beats vs. 7.8 ± 0.4×10^?3 min/beats, p<0.01). Although treatment with amlodipine alone did not abolish the circadian pattern of minimal coronary vascular resistance (8.0 ± 0.6×10^?3 min/beats vs. 7.7 ± 0.6×10^?3 min/beats, p<0.05), the addition of prazosin virtually eliminated the diurnal difference in minimal coronary vascular resistance (7.4 ± 0.5×10^?3 min/beats vs. 7.5 ± 0.5×10^?3 min/beats, p = NS). Conclusions: These findings indicate that α₁-sympathetic activity may play a role in the pathogenesis of the diurnal change of ischemic threshold in patients with stable angina.