丙泊酚对缺血-再灌注心肌中钙激活蛋白酶表达及细胞凋亡的影响

目的 观察丙泊酚对缺血-再灌注损伤心肌细胞中m型钙激活蛋白酶（m-calpain）的表达和细胞凋亡的影响，探讨丙泊酚减少缺血-再灌注损伤心肌细胞凋亡的机制.方法 4月龄健康雄性新西兰大耳白兔24只，体重2.1～2.3 kg，随机分为三组：假手术组（Sham组）、缺血-再灌注组（I-R组）和丙泊酚组（P组），每组8只.实验结束取缺血区心肌标本，免疫组织化学方法（SP法）检测m-calpain的表达，Motic 6.0图像分析系统进行处理，采集平均光密度值（AO值）进行统计分析；Annexin Ⅴ-PI双染色法、TUNEL法测定细胞凋亡.结果 Sham组心肌组织中m-calpain低表达，Annexin Ⅴ-PI双染色法、TUNEL染色检测有少量凋亡细胞；与Sham组比较，P组、I-R组m-calpain表达增加（P＜0.05），Annexin Ⅴ-PI双染色检测早期凋亡细胞和TUNEL染色阳性细胞增加（P＜0.05）；与I-R组比较，P组m-calpain表达下降（P＜0.05），Annexin Ⅴ-PI双染色检测早期凋亡心肌细胞减少（P＜0.05）、TUNEL阳性细胞减少（P＜0.05）.结论 丙泊酚可抑制心肌缺血-再灌注损伤时m-calpain的激活，减少缺血-再灌注心肌细胞凋亡.     

99Tcm-MIBI动力学变化与大鼠缺血-再灌注心肌存活的相关性研究

目的探讨用99Tcm-甲氧基异丁基异腈(MIBI)动力学变化评价心肌存活的价值.方法15只离体Krebs-Henseleit(KH)液灌注的鼠心脏,随机分成3组对照组(5只),有葡萄糖的缺血-再灌注组(IR+G组,5只),无葡萄糖的缺血-再灌注组(IR-G组,5只).用含99Tcm-MIBI(14.8MBq)的KH液灌注,观察40min的摄取和清除.用肌酸激酶(CK)分析、氯化三苯四唑(TTC)染色和透射电镜(TEM)分析研究心肌损伤程度,用放射自显影(ARG)观察99Tcm-MIBI在心肌内的分布.结果99Tcm-MIBI的摄取[每克组织百分注射剂量率(%ID/g)]在IR+G组为(7.09±0.97)%ID/g,IR-G组为(6.64±0.68)%ID/g,对照组为(11.44±1.79)%ID/g,IR-G组与IR+G组相比摄取量差异无显著性(P＞0.05),IR-G组和IR+G组与对照组相比均显著降低(P＜0.05).IR-G组99m-MIBI清除分数为(72.75±9.89)%,远高于对照组[(20.68±1.92)%]和IR+G组[(21.03±3.68)%,P均＜0.05],对照组与IR+G组的差异无显著性.99Tcm-MIBI的40min清除末滞留率在IR-G组[(1.82±0.73)%ID/g]和IR+G组[(5.61±0.89)%ID/g]远小于对照组[(9.09±1.57)%ID/g,P＜0.05],IR-G组也远小于IR+G组(P＜0.001).CK分析、TFC染色和TEM分析证明IR-G组比IR+G组有更多的心肌损伤.通过TTC染色(r=0.84,P＜0.05)和CK分析(r=-0.97,P＜0.05)确定最终99Tcm-MIBI的活度与存活心肌量高度相关,通过ARG证实99Tcm-MIBI分布于鼠心肌细胞及间质内(光镜下).结论99Tcm-MIBI的清除对代谢状态敏感,可用于评价进行性心肌损伤.     

Mortality risk associated with ejection fraction differs across resting nuclear perfusion findings

Background  Left ventricular ejection fraction (LVEF) is a significant predictor of morbidity and death. The nuclear summed rest score (SRS) measures myocardial perfusion defects and provides prognostic information, but its effects on long-term outcomes are not fully established. Moreover, information regarding the potential interaction between these 2 covariates is limited. The purpose of this study was to determine whether the mortality risk associated with LVEF is the same across all values of SRS in a population undergoing evaluation for ischemic heart disease. Methods and Results  We examined 3,187 patients who underwent cardiac catheterization and perfusion single photon emission computed tomography imaging with a maximum follow-up of 8.1 years and median follow-up of 3.1 years. Cox proportional hazards modeling showed that increasing nuclear SRS and decreasing LVEF were independently associated with a higher long-term mortality rate, with a clinically significant interaction between them (P=.032). Patients with a normal LVEF and a high SRS (greater perfusion abnormality) have a prognosis similar to those with a reduced LVEF. Conclusions  Resting perfusion studies provide prognostic information for long-term survival and significantly impact the interpretition of mortality risk associated with changes in LVEF. Patient prognostication, risk stratification, and future research using these variables should take this interaction into account. Supported by a grant from the Tom & Lynn Royster Foundation. Durham, NC, and a National Institutes of Health Research Fellowship Grant (T5 GM08679-04), Bethesda, Md.     

心肌显像联合冠状动脉造影及组织学检查在评价Ad-HGF治疗猪心肌梗死疗效中的价值

目的探讨心肌静息显像联合冠状动脉造影及组织学检查在评价重组腺病毒-肝细胞生长因子（Ad—HGF）治疗猪实验性心肌梗死中的价值。方法低、中、高剂量Ad—HGF治疗组[Ad-HGF剂量依次为10^8，4×10^8，5×10^9空斑形成单位（PFU）／点；均分10点注射]，生理盐水对照组及空白对照组小型猪各5头，分别于治疗前后行静息心肌显像及冠状动脉造影，并于治疗后行组织学检查。结果空白对照组及生理盐水对照组治疗前后心肌灌注及Rentrop评分无明显变化。各Ad-HGF治疗组治疗后心肌灌注及Rentrop评分较治疗前改善，低、中、高剂量组治疗前后冠状动脉左回旋支（LCX）供血节段得分分别为7．8±1．3和16．4±1．1（低），8．2±1．6和17．6±0．9（中），8．4±1．5和19．0±0．7（高）；各组治疗前后LCX供血区域Rentrop评分分别为0．80±0．16和1．66±0．15（低），0．94±0．11和2．16±0．11]（中），0．90±0．22和2．22±0．19（高）。3组治疗前后数据比较差异均有统计学意义（P〈0．01）。各Ad-HGF治疗组及空白对照组治疗后血管数量明显多于生理盐水对照组。结论用心肌静息显像联合冠状动脉造影及组织学检查评价Ad-HGF治疗猪心肌梗死的疗效有价值。     

阿片受体对体外循环缺血再灌注损伤心肌的保护作用

目的 通过建立猪体外循环(CPB)心肌缺血再灌注(MI/R)模型对δ阿片受体激动剂脑腓肽(DADLE)介导的CPB MI/R损伤早期时相和后时相的心肌保护作用进行探讨,以期为临床心肌保护提供理论和实验依据.方法 将24只成年家猪随机分为对照组、早期时相和后时相组,每组8只常规建立CPB模型,主动脉阻断同时灌注改良St.Thomas停搏液.每组于CPB前、主动脉开放时、CPB结束时、停机后1、2 h检测冠状静脉窦血肌钙蛋白(TnT)含量,相应时间点监测左室舒张末期压(LVEDP)和左室内压最大变化速率(±ap/dt<,max>),于停机后2h取左心室心肌,进行心肌组织Gia蛋白的表达、PKC的表达和ATP含量的测定.并应用透射电镜观察心肌再灌注损伤超微结构的变化.结果 (1)和早期时相和后时相组相比,对照组心功能指标明显下降.(2)对照组的TnT较早期时相和后时相组明显升高,ATP含量明显降低.(3)和对照组相比,早期时相和后时相组Gin蛋白和PKC的表达更为明显.(4)透射电镜下早期时相和后时相组的心肌超微结构损伤均较对照组明显轻微.结论 (1)和CPB前1 h应用一次DADLE而产生的早期时相心肌保护作用相比,CPB前48 h和24 h两次应用DADLE引发的后时相心肌保护作用更为显著.(2)Gi蛋白-PKC途径可能是δ阿片受体介导的猪CPB NI/R损伤心肌保护中一条重要的信号传导途径.     

光学相干断层成像技术判断心肌缺血损伤程度和范围在体研究的进展

外科手术对心肌缺血的血运重建是目前治疗心肌缺血性疾病的重要手段之一。术中准确判断心肌缺血范围及程度和严密监测心脏停跳后心肌细胞损伤是否加重，对于血运重建的准确性，更好地实施心肌保护及对手术疗效的评估和术后处理方案的拟定有着重要意义。因此，如何在术中判断心肌缺血的损伤程度和范围具有极为重要的实验研究意义与临床现实意义。光学相干层析成像作为一种新颖的成像技术，能对活体组织内部微小结构进行实时、在体、高分辨率断层成像。     

急性心肌梗死患者J波的临床研究

目的　研究心电图有 J波的急性心肌梗死 ( AMI)患者的临床情况。方法　选择住院的急性心肌梗死患者 10 2例 ,心电图有 J波者 5 0例为研究组 ,心电图无 J波者 5 2例为对照组 ,比较两组临床情况。结果　心电图有 J波组比心电图无 J波组发生胸闷 ( 3 0 /5 0∶ 2 0 /5 2 ,P<0 .0 5 )、前壁心肌梗死 ( 2 8/5 0∶ 18/5 2 ,P<0 .0 5 )、合并糖尿病 ( 14/5 0∶ 4/5 2 ,P<0 .0 5 )、超声心动图检查发生舒张功能减低 ( 2 4/5 0∶ 14/5 2 ,P<0 .0 5 )、心电图检查发现室性心动过速 ( 11/5 0∶ 1/5 1,P<0 .0 5 )者多。结论　心电图有 J波者比心电图无 J波者临床情况差 ,易于发生严重心律失常     

Heart failure: Effects of beta receptor antagonists on left ventricular function in patients with clinical evidence of heart failure after myocardial infarction. A double-blind comparison of metoprolol and xamoterol Echocardiographic results from the Metoprolol and Xamoterol Infarction Study (MEXIS)

Two hundred and ten patients with clinical evidence of heartfailure, developing after an acute myocardial infarction, wererandomized to treatment with the ß₁ antagonist metoprolol50–100mg b.i.d. (n=106) or the ß₁ partial agonistxamoterol 100–200 mg bid. (n=104). Left ventricular systolicand diastolic function were assessed with echocardiography andtransmitral Doppler cardiography before and after 3 and 12 monthsof double-blind treatment. E-point septal separation and percent left ventricular fractional shortening were used as indicesof systolic function. The ratio between peak early and latemitral diastolic flow (E/A ratio) and isovolumic relaxationtime were used as indices of diastolic function. In the xamoterol group, there was a deterioration in E-pointseptal separation (P<0·05). A difference between thetreatment groups was present both at 3 months (E-point septalseparation 11·4 vs 13·0 mm, P<0·0l,fractional short ening 271 vs 252%, P<005) and 12 months(E-point septal separation Ill vs 13·2 mm, P<0·05fractional shortening 26·9 vs 25·0%, P<0·05).E/A ratio increased in the metoprolol group (P<0·05)but not in the xamoterol group. At 3 months there was a significantdifference (0·85 vs 0·67, P<0·005 betweenthe groups but not at 12 months. In comparison with the ß₁-receptor antagonist metoprolol,the ß₁ partial agonist xamoterol impaired left ventricularsystolic function in patients with clinical evidence of heartfailure after an acute myocardial infarction.     

ADM对LNNA诱导的高血压心肌肥大的作用及机制探讨

本工作在ＬＮＮＡ经慢性ＮＯ封闭诱导的大鼠高血压心肌肥大模型上研究了ＡＤＭ对其心肌肥大和Ｍ５ＬＶ钠一钙交换功能损伤的作用。结果：一、较之对照组，ＬＮＮＡ组ＭＡＯ和ＬＶＩ分别增加５７．４％和１８。０％（Ｐ＜０．０１）．其ＭＳＬＶ经钠－钙交换蛋白的钙摄取则明显降低（Ｐ＜０．０１或０．０５）：二．ＡＤＭ组的ＭＡＰ和ＬＶＩ则分别较ＬＮＮＡ组降低１９．６％和１１．３％，而其ＭＳＬＶ的钙摄取则高于ＬＮＮＡ组（Ｐ＜０．０５）；三、对照组、ＬＮＮＡ组和ＡＤＭ组钠－钙交换蛋白摄取钙的Ｋｍ值分别为７．５１．７．０４和７．５７ｕＭ，而Ｖｍａｘ则分别为６．３８，４．３２和５．４５ｎｍｏｌ／。ｍｇｐｒ／ｍｉｎ。表明：ＡＤＭ能拮抗ＬＮＮＡ诱导的高血压心肌肥大和减轻其ＭＳｌｌＶ钠－钙交换功能的损伤，并且后者可能是ＡＤＭ拮抗心肌肥大的机制之一。揭示内源性ＡＤＭ的诱导和外源性给予ＡＤＭ可能有预防和／或延缓高血压心肌肥大发生发展的作用。