麝香保心片对心肌缺血缺氧的保护作用

目的：观察麝香保心片对实验性心肌缺血的药理效应。方法：用垂体后叶素造成大鼠急性心肌缺血模型，观察麝香保心片对心电图T波的影响；用腹腔注射异丙肾上腺素造成小鼠急性心肌缺血模型，观察麝香保心片对小鼠心肌组织丙二醛含量及心肌酶谱的影响。结果：麝香保心片组与模型组相比，可以显改善心电图缺血性改变（P＜0．05）；减少心肌组织丙二醛的生成（P＜0．01），抑制心肌AST、LDH、CPK、CK－MB的升高。结论：麝香保心片可以有效改善冠脉循环，保护缺血心肌。     

心肌缺血的运动心电信号无创检测方法

目的 改进用于心肌缺血无创检测的运动心电信号特征分析方法。方法研制一套改进的运动心电信号检测系统，提出单位时间ＳＴ段面积（ＳＴＡ）和ＳＴＡ与相关心率（ＳＴＡ／ＨＲ）的斜率作为新特征参数的计算方法，同时还提出了减少运动信号采集中干扰噪声混入的措施。结果 临床运动试验中采集到的１４例运动心电信号数据特征所进行的分析结果，验证了这些新参数计算的有效性头痛的计算结果不仅计算基本一致，而且提高了运动心电信号     

双参素胶囊对大鼠实验性心肌缺血再灌注损伤的保护作用

 目的 观察双参素胶囊对大鼠实验性心肌缺血再灌注损伤的保护作用.方法 通过在体大鼠结扎左冠状动脉前降支30min,再灌注24 h制备实验性心肌缺血再灌注损伤模型,双参素胶囊按17.5mg/kg、35 mg/kg、70 mg/kg给大鼠连续灌胃7 d,阳性药物组连续灌胃福辛普利20 mg/kg,7 d,假手术组及再灌模型组灌胃0.5%羧甲基纤维素钠,计算心肌梗死范围(MIS),测定血清天冬酸氨基转移酶(AST)等的活性.结果　双参素胶囊可使实验性心肌缺血再灌注损伤大鼠的MIS明显缩小(P＜0.05或P＜0.01),血清AST、LDH、CK-MB活性及MDA含量明显降低(P＜0.05或P＜0.01),血清SOD及GSH-Px活性明显增加(P＜0.05或P＜0.01),亦可使血浆ET和AngⅡ含量明显下降(P＜0.05或P＜0.01).结论 双参素胶囊对大鼠实验性心肌缺血再灌注损伤具有明显保护作用.     

血脂康对血脂正常心绞痛患者抗心肌缺血作用的研究

本文对他汀类药物血脂康与血脂正常的冠心病(CHD)患者心肌缺血的关系进行了研究,以探讨血脂康对CHD患者是否具有抗缺血作用。     

麝香保心丸治疗无症状心肌缺血疗效观察

目的：观察麝香保心丸治疗无症状心肌缺血的临床疗效及不良反应。方法：选择无症状心肌缺血80例,随机分为观察组与对照组各40例。观察组采用麝香保心丸治疗,每次2粒,每天3次;对照组采用硝酸异山梨酯治疗,每次10mg,每天3次。两组均治疗4周。比较两组心电图缺血、各种期前收缩、血流动力学、血脂变化等。结果：观察组心电图改善37例（92.5%）,对照组30例（75.0%）,两组比较差异显著（P〈0.05）;观察组各种期前收缩、血流动力学、血脂等改善情况显著好于对照组（P〈0.05）。两组均未发现严重不良反应。结论：麝香保心丸治疗无症状心肌缺血疗效可靠,且安全。     

圣脑康丸对大鼠急性心肌缺血模型心电图的影响

目的研究圣脑康丸对大鼠急性心肌缺血模型心电图的影响。方法各给药组大鼠先给相应药物7 d进行预处理,然后尾静脉注射垂体后叶素制备大鼠急性心肌缺血模型,检测注射垂体后叶素后不同时间点的Ⅱ导联心电图ST段、T波及心率的变化。结果圣脑康丸对垂体后叶素诱发的大鼠急性心肌缺血的心电图中心率、ST段和T波的改变有一定的抑制作用。结论圣脑康丸对大鼠急性心肌缺血模型心电图的改变有一定的抑制作用,对大鼠急性心肌缺血具有较好的改善作用。     

细胞保护作用的抗心肌缺血药物研究进展

目前，药物治疗仍然是临床上治疗心肌缺血的主要手段，主要治疗药物包括硝酸酯类、β—受体阻滞剂和钙拮抗剂等。上述药物通过减轻心脏负荷、提高心脏供氧等间接途径发挥保护作用，因此，其疗效以及临床应用均受到一定限制。近年来，随着心血管药理学研究的逐步深入，人们发现几类具有明确抗心肌缺血作用的新药。这些药物直接在细甩水平发挥保护作用，不影响血流动力学。根据作用机理可分为预适应保护药物和代谢治疗药物，前者通过激活心肌内源性保护系统发挥作用；后者直接改善心肌细胞代谢状态。具有较高的研究意义和开发价值。此外，两类药物均通过保护心肌线粒体结构和功能发挥保护作用．深入研究其作用机理和相互关系．有可能获得更深层次的发现。     

舒血宁注射液对大鼠心肌缺血再灌注损伤的保护作用

目的观察舒血宁对大鼠心肌缺血再灌注（MIR）损伤后的保护作用。方法30只SD雄性大鼠随机分成假手术组、手术组和舒血宁组。采用结扎左冠状动脉前降支（LAD）复制大鼠心肌缺血再灌注损伤模型,用氯化三苯四唑（TTC）染色法测定心肌梗死面积,测定血浆肌酸激酶（CK—MB）和肌钙蛋白I（cTnI）浓度水平以及心肌组织NO的含量。结果与手术组相比,舒血宁组心肌梗死面积明显减少,并能显著降低血清CK～MB、cTnI浓度以及提高心肌组织NO的含量。结论舒血宁对心肌缺血再灌注损伤有明显的保护作用,可能与提高心肌NO的含量有关。     

滇丹参提取液对心肌缺血大鼠血液流变性的影响

目的：探讨云南产甘西鼠尾属药物滇丹参对大鼠血液流变性的影响.方法：结扎大鼠冠状动脉左前降支造成急性心肌梗塞模型,股静脉给药,1.5 h后颈动脉取血测定全血粘度、血浆粘度、红细胞压积、血浆纤维蛋白原含量等血液流变学指标.结果：滇丹参10 g/kg、4 g/kg、2 g/kg三种剂量均能显著降低高、中、低切变率下的全血粘度和血浆粘度（P＜0.01,P＜0.05）,能显著降低纤维蛋白原含量（P＜0.01）;10 g/kg时,能降低红细胞压积（P＜0.01,P＜0.05）.结论：滇丹参具有改善心肌缺血大鼠血液流变异常的作用.     

抗心肌缺血药物对核素心肌灌注显像的影响

冠状动脉粥样硬化性心脏病简称冠心病(coronary heart disease,CAD),已成为危害人类健康的重要杀手,因此早期、准确地诊断冠心病至关重要。核素心肌灌注显像(myocardial perfusion imaging,MPI)是诊断CAD重要的无创性检查方法,     

刺囊酸对异丙肾上腺素诱导大鼠心肌缺血损伤的影响

目的：观察刺囊酸对异丙肾上腺素（ISO）诱导大鼠心肌缺血损伤的影响。方法：将30只健康雄性sD大鼠随机等分为对照组（S）、异丙肾组（I）、刺囊酸＋异丙。肾（E）组,并造模给药。给ISO后24h,麻醉处死动物。测定血清肌酸激酶（CK）、乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）、丙二醛（MDA）表达。HE染色后在光镜下观察心肌组织形态学改变。结果：和I组比较,E组血清中LDH、CK和MDA含量明显降低（P〈0．01）,SOD的活力明显升高（P〈0．01）。E组大鼠心肌病变的程度较I组减轻较明显。结论：刺囊酸对ISO诱导大鼠缺血损伤的心肌具有一定的保护作用。     

腺苷对心肌缺血再灌注心律失常的保护作用

目的观察腺苷对在体大鼠心肌缺血／再灌注（I／R）心律失常的影响，探讨其可能的作用机制。方法健康Wister大鼠36只，随机分成3组假手术组、对照组、腺苷组，每组12只。开胸结扎左冠状动脉前降支30分钟，再灌注45分钟．制作大鼠心肌缺血／再灌注损伤模型。假手术组只穿线不结扎冠状动脉。腺苷组于结扎前1分钟给予腺W（0．4ml／kg）左心室内注入，对照组给予等量生理盐水左心室内注入。观察再灌注室性心动过速（VT）、室颤（VF）发生率和死亡率；检测左心室心肌组织超氧化物歧化酶（SOD）及丙二醛（MDA）含量。结果①腺苷组大鼠再灌注VT及VF发生率及死亡率均较对照组明显降低（P〈0.01）；②与对照组比较，腺苷组大鼠SOD活力提高（P〈0．05），而MDA生成量明显减少（P〈0．01）。结论心肌缺血再灌注可导致缺血心肌进一步损伤，腺苷具有抗大鼠I／R心律失常作用，可能与抑制缺血再灌注氧自由基的产生有关。     

Swim training improves myocardial resistance to ischemia in rats

As the relationship between training and ischemic heart disease is not yet unraveled, we test the hypothesis that, in a model free from environmental, behavioural, and neuro-hormonal factors, endurance training improves myocardial resistance to ischemia. As carbohydrate metabolism is relevant for myocardial resistance to ischemia, we also test whether hyperglycemia blunts the protective effect of training. Eight-week old rats were randomly assigned to four groups (n = 6-8): sedentary or trained (3-week swim program, up to 2 h/day), and normal or high-carbohydrate diet (50 g/l sucrose in drinking water). Excised hearts were perfused isovolumically (flow = 15 ml/min) with Krebs-Henseleit (2 mM free Ca++, 11 mM glucose, pH 7.38 +/- 0.02, PO2 = 670 +/- 6 mmHg, PCO2 = 43 +/- 1 mmHg, mean +/- SE), exposed to 60 min low-flow (1.5 ml/min) ischemia, and then reperfused for 30 min (15 ml/min). In normally fed rats training increased the stroke volume index (97.5 +/- 13.0 vs. 72.6 +/- 6.2 microl, P = 0.05), depressed diastolic contracture (+2.3 +/- 2.0 vs. +24.2 +/- 6.7 mmHg, P = 0.02), improved the recovery of developed pressure x heart rate (33.8 +/- 2.3 vs. 24.1 +/- 3.3 mmHg/min/1000, P = 0.05), and decreased arrhythmias (P = 0.05). In high-carbohydrate-fed rats training induced myocardial hypertrophy (1.95 +/- 0.08 vs. 1.67 +/- 0.03 g, P = 0.02) and decreased arrhythmias but did not affect stroke volume, developed pressure x heart rate, and diastolic contracture. Thus endurance training improves myocardial resistance to ischemia but a high-carbohydrate diet partially blunts this protection. The occurrence of an inducible alteration able to modulate myocardial tolerance to ischemia may give clues to extend our knowledge of ischemic preconditioning.     

The contrast of immunohistochemical studies of myocardial fibrinogen and myoglobin in early myocardial ischemia in rats

In this study, an animal model of early myocardial ischemia (EMI) was established by ligating the left anterior descending coronary artery of rats. The experimental animals were divided into five groups according to different intervals of MI (15, 30min, 1, 2, and 3h) and one control group. Tissues from the apex of the myocardium and the adjacent myocardium were taken for paraffin sections, followed by hematoxylin-eosin and streptavidin-biotin-peroxidase complex (SABC) staining. Results showed that the myoglobin (Mb) depletion and the fibrinogen (Fg) staining increase were detected in the 30min MI group. The wavy-like increasing extension of the size and the intensity of the Mb depletion and the Fg staining intensification from the subendocardial to the subepicardial cells were observed along with the prolongation of the ischemic period. Both changes had similar patterns and sensitivity, except Fg was less reliable than Mb as it is more easily contaminated by blood. After overcoming blood contamination, the SABC-Fg technique will provide a new method for the diagnosis of EMI.     

柚皮素预处理对心肌缺血/再灌注损伤大鼠能量代谢的影响

 目的 探讨柚皮素预处理对心肌缺血/再灌注损伤大鼠能量代谢的影响。方法 将大鼠随机分为5组(n=10):假手术组、模型组,柚皮素分为三个剂量组(100、50、25 mg/kg),于建立模型前7 d开始腹腔注射给药,通过结扎冠脉30 min再灌注2 h建立心肌缺血/再灌注损伤模型;再灌注结束后,采用比色法测定血清肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,采用定磷法测定心肌组织Na^＋/K^＋-ATP酶和Ca²⁺/Mg²⁺-ATP酶的活力,采用染色法测定心肌梗死面积(myocardial infarction surface, MIS)。结果 柚皮素高剂量组MIS缩小至32.91%,与模型组MIS(39.78%)比较差异有统计学意义(P<0.05);柚皮素各剂量组CK活性分别降低为658.03、650.12、621.89 U/L,与模型组(809.45 U/L)比较,差异均有统计学意义(P<0.05或P<0.01);各剂量组LDH活性分别降低为1543.08、1506.27、1326.97 U/L,与模型组(2034.56 U/L)比较差异均有统计学意义(P<0.05或P< 0.01);柚皮素各剂量组可显著升高Na^＋/K^＋-ATP酶活力为6.82、6.83、6.94 mmol Pi/(g·h),与模型组[5.54 mmol Pi/(g·h)]比较差异均有统计学意义(P<0.05);高、中剂量组可显著升高,Ca²⁺/Mg²⁺-ATP酶活力为8.42、8.97 mmol Pi/(g·h),与模型组[7.06 mmol Pi/(g·h)]比较差异均有统计学意义(P<0.05)。结论 柚皮素预处理对心肌缺血/再灌注所致心肌损伤的保护作用可能与改善心肌组织的能量代谢有关。     

参麦注射液对大鼠心肌缺血/再灌注心律失常的影响

目的探讨参麦注射液对大鼠缺血/再灌注心律失常的影响及其作用机制。方法复制大鼠缺血/再灌注模型,采用缺血10min和缺血60min两种模型观察缺血性心律失常,观察发生率最高的缺血10min后再灌注心律失常,对照组和参麦注射液组分别给予生理盐水和参麦注射液1.5ml/kg,动态Ⅱ导心电图监测室性早搏（PVB）、室性心动过速（VT）及心室颤动与扑动（VF）的发生率。结果参麦注射液可明显减少缺血10min和60min心律失常PVB、VT、VF的发生率（P〈0.01）,亦可明显减少再灌注10min心律失常VT（P〈0.05）及VF（P〈0.01）的发生率。结论参麦注射液可明显减少大鼠缺血/再灌注心律失常的发生率。     

粉防己碱对大鼠肝脏缺血和再灌注损伤的防护作用

目的 观察粉防己碱（Ｔｅｔ）对大鼠肝再灌注损伤的防护作用及其机制。方法 （１）Ｆｕｒａ－２／ＡＭ检测Ｔｅｔ对离体肝细胞游离钙离子浓度（［Ｃａ＾＋２］ｉ）的影响。（２）制作大鼠缺血再灌注损伤模型，将实验大鼠随机分为对照组（Ｃｔｒｌ，鼠数＝３５）、粉防己碱（Ｔｅｔ）组（鼠数＝３５）和假手术组（Ｓｈａｍ，鼠数＝５）。Ｔｅｔ组大鼠按８ｍｇ／ｋｇ Ｔｅｔ于缺血前、再灌注前静脉注射，动态观察血清谷丙转氨酶（Ａ     

SP600125对大鼠脑缺血再灌注神经元的保护作用

目的探讨SP600125-JNK特异性抑制剂对大鼠脑缺血再灌注神经元损伤的保护性作用及其作用机制。方法雄性SD大鼠54只,体重230～250g,随机分成假手术组（SH组）,缺血再灌注组（IR组）和JNK抑制剂SP600125组（SP组）,每组根据再灌注时间分为30min、24h和72h3个亚组,每亚组6只动物。采用4-VO法建立SD大鼠脑缺血模型,三组于缺血前30min侧脑室注射DMSO,DMSO及JNK抑制剂SP600125（溶媒采用DMSO）,容积均为10μl;脑缺血再灌注后30min、24h、72h免疫组织化学方法测定各时间点海马CA1区Bcl-2和Bax蛋白表达阳性细胞数量,TUNEL法检测CA1区凋亡细胞。结果缺血再灌注使海马CA1区Bcl-2和Bax阳性锥体细胞数目表达增加,再灌注24h阳性锥体细胞数目表达至高峰（P〈0.01）,再灌注24～72h可见阳性锥体细胞数目表达减少（P〈0.05）。其中SP组Bcl-2阳性锥体细胞数目显著多于IR组（P〈0.05）,而Bax阳性锥体细胞数目显著小于IR组（P〈0.05）。脑缺血再灌注后海马CA1区神经元存活数目SP组高于IR组（P〈0.01）,凋亡细胞数目低于IR组（P〈0.01）。结论 SP600125对大鼠脑缺血再灌注神经元损伤具有保护作用。     

辛伐他汀预处理减轻缺血再灌注心肌损伤的实验研究

Objective To investigate the effects of pretreatment with simvastatin on iscbemia reperfusion induced myocardial injury, and to further explore related mechanism with respect to inflammation modulation. Methods The rat myocardial ischemia reperfusion model was established by the method of coronary artery ligation. The animals were divided into 3 groups: the sham group, the control group and the simvastatin group. In the simvastatin group, the animals were pretreated with simvastatin (5 mg/kg) one week before by intragastric administration. Ventricular arrhythmia was monitored and scored, infarct size and area at risk of myocardium were determined, and uhrastructural changes were observed. The serum levels of myocardial enzymes and lipids were measured. The content of myocardial inflammatory cytokines [tumor necrosis factor (TNF) -α、interleukin(IL) -6, and monocyte chemoattractant protein(MCP) - 1]were also evaluated. Results When compared with those of the control group, the amount and duration of ventricular arrhythmia in simvastatin group were less and score of ventricular arrhythmia was significantly lower. When pretreated with simvastatin, the serum levels of CK-MB and LDH in simvastatin group were significantly lower than those of the control group. The infarct size/area at risk ratio of the simvastatin treated group was significantly less than those of the control group. The uhrastructures of myocardial cells were better maintained in simvastatin group. No significant differences were observed in the serum concentrations of total cholesterol, triglycerides, low density lipoprotein and high density lipoprotein when comparisons were made each other among the three groups. However, the levels of TNF-α,IL-6 and MCP-1 in heart tissue of the treated animals were significantly lower than those of the control group. Conclusions Pretreatment with simvastatin ameliorates ischemia reperfusion induced myocardial injury, which is partly related with the down-regulation of inflammatory cytokines expression in heart tissue but independent of its role of lipids modulation.     

牛磺酸对大鼠局灶性脑缺血再灌注损伤的保护作用

目的研究牛磺酸(Taurine)对大鼠局灶性脑缺血再灌注损伤的影响并探讨其机制。方法采用大鼠大脑中动脉梗死(MCAO)模型,将大鼠随机分为假手术组(Sham)、缺血再灌注组(I/R)和缺血再灌注加牛磺酸处理组(I/R+Taurine),观察缺血1 h再灌注24 h后,各组大鼠脑梗死体积、脑水含量及核因子кB(NF-кB)P65表达的变化。结果3组大鼠脑梗死体积百分比分别为0(、13.32±3.18)%(、9.21±2.24)%,与单纯缺血再灌注组比较,牛磺酸处理组脑梗死体积减少30.83%(P<0.05);脑水含量分别为(79.28±0.66)%,(82.46±0.94)%,(80.73±1.40)%,给药组脑水肿明显减轻(P<0.05);免疫组化染色结果显示牛磺酸抑制NF-кB的表达(P<0.05)。结论牛磺酸对大鼠局灶性脑缺血再灌注损伤具有保护作用,该作用与其抑制NF-кB的激活,减轻神经细胞损害有关。