迷走神经在电针提高急性心肌缺血早期室颤阈中的作用

目的 通过动物实验观察电针对急性心肌缺血所致的ＶＦＴ降低的影响,分析探讨迷走神经在电针提高ＶＦＴ中的作用机制。方法 用结扎兔冠脉建立急性心肌缺血动物模型,观察比较对照组、电针组、切断迷走神经组等室颤阈值、血浆ｃＡＭＰ、ｃＧＭＰ,并对其心率变异频谱特征进行分析。结果 实验显示电针能显示提高缺血心肌的ＶＦＴ（Ｐ〈０．０５,Ｐ〈０．０１）;切断迷走神经后,电针的这一作用消失（Ｐ〈０．０５,Ｐ〈０．０１）     

电针对急性心肌缺血家兔心功能及心交感神经电活动的影响

目的:通过观察电针不同经穴对急性心肌缺血家兔心功能及心交感神经放电的影响,探讨原、络穴作用的相对特异性。方法:50只家兔随机分为正常对照组、模型对照组、电针神门组和电针支正组,采用静脉注射脑垂体后叶素复制急性心肌缺血模型。用Biopac生物信号采集系统记录神经电信号和心功能各指标;同时接入SKY-A4生物信号处理系统进行统计分析,记录电针"神门"支正"穴前后急性心肌缺血家兔心功能及心交感神经电活动的变化。结果:电针神门组、电针支正组在停针即刻心功能指标和心交感神经电活动与模型对照组比较均有统计学意义(P<0.05)。两组间比较,电针神门组各项指标改善优于电针支正组(P<0.05)。结论:电针"神门"支正"穴均可显著改善急性心肌缺血家兔的心功能并可提高心肌缺血状态下心交感神经的兴奋性,且电针"神门"穴的作用优于"支正"穴。     

Cardioprotective effects of saponins from Panax japonicus on acute myocardial ischemia against oxidative stress-triggered damage and cardiac cell death in rats

Aim

To study the cardioprotective effects of saponins from Panax japonicus (SPJ) on acute myocardial ischemia injury rats induced by ligating of the left anterior descending branch (LAD), on the basis of this investigation, the possible mechanism of SPJ was elucidated.

Materials and methods

SPJ was identified by high performance liquid chromatography-evaporative light scattering detection. Male Sprague-Dawley rats (200–220 g) were randomly divided into four groups: sham-operated, LAD, LAD + l-SPJ (SPJ, 50 mg/kg/day, orally) and LAD + h-SPJ (SPJ, 100 mg/kg/day, orally). Before operation, the foregoing groups were pretreated with homologous drug once a day for 7 days, respectively. After twelve hours in LAD, the cardioprotective effects of SPJ were evaluated by infarct size, biochemical values, hemodynamic, and histopathological observations and the antioxidative and antiapoptotic relative gene expressions.

Results

SPJ significantly improved heart function and decreased infarct size; remarkably decreased levels of serum lactate dehydrogenase, creatine kinase, xanthine oxide and malondialdehyde content, increased contents of serum total antioxidant capacity, superoxide dismutase (SOD), glutathione peroxidase, catalase; quantitative real-time PCR results showed that SPJ might markedly reverse the down-regulated mRNA expressions of the SOD1, SOD2 and SOD3, ameliorate the increased Bax and caspase-3 mRNA expressions and decreased Bcl-2 mRNA expression and ratios of Bcl-2 to Bax. Histopathological observations provided supportive evidence for biochemical analyses, and with the dose of SPJ increasing, the aforesaid improvement became more and more strong.

Conclusions

The studies demonstrated that in ischemic myocardium, oxidative stress caused the overgeneration and accumulation of reactive oxygen species (ROS), which was central of cardiac ischemic injury. SPJ exerted beneficially cardioprotective effects on myocardial ischemia injury rats, mainly scavenging oxidative stress-triggered overgeneration and accumulation of ROS, alleviating myocardial ischemia injury and cardiac cell death.     

头针对心肌缺血再灌注大鼠心交感放电、心肌β_1-肾上腺素受体蛋白表达及血浆去甲肾上腺素含量的影响

目的:观察头针"额旁1线"对心肌缺血再灌注损伤大鼠交感神经活动、心肌β1-肾上腺素受体(β1-AR)蛋白表达及血浆去甲肾上腺素(NE)含量的影响,探讨头针防治心肌缺血再灌注损伤的作用机制。方法:Wistar大鼠随机分成假手术组、模型组、头针组,每组6只。采用结扎左冠状动脉前降支30min,再灌注15min制备大鼠心肌缺血再灌注模型。取头部双侧"额旁1线"区域进行电针治疗,频率14Hz,强度为2V。用BL-420E+生物信号采集系统记录左交感神经放电情况,通过免疫印迹法检测缺血区心肌β1-AR蛋白表达变化,利用酶联免疫吸附法测定血浆NE含量的变化。结果:模型组和头针组大鼠在缺血30min和再灌注15min后,交感神经放电频率较缺血前及假手术组明显加快(P<0.01,P<0.05),而头针组较模型组明显减慢(P<0.05)。模型组大鼠心肌β1-AR蛋白表达增加,血浆NE含量明显上升,与假手术组比较差异有统计学意义(P<0.01);头针组大鼠缺血区心肌β1-AR蛋白表达显著下调,血浆NE浓度明显降低,与模型组比较差异有统计学意义(P<0.05)。结论:头针可通过调整心肌缺血再灌注大鼠交感神经放电频率、心肌β1-AR蛋白表达水平及血浆NE含量,减轻钙超载,使紊乱的心肌细胞电活动趋于和缓,发挥其抗再灌注心肌损伤作用。     

人参Rb组皂苷对实验性心肌梗死犬心脏血流动力学及氧代谢的影响

目的：研究人参Rb组皂苷对急性心肌梗死犬心脏血流动力学及氧代谢的影响。方法：采用麻醉开胸犬结扎左冠状动脉前降支（LAD）产生急性心肌梗死模型，测定心脏血流动力学、冠状循环及氧化代谢等参数。结果：人参Rb组皂苷25，50mg/kg经十二指肠给药，对结扎LAD产生急性心肌梗死6h犬，均能明显减慢心率（HR），降低MAP、＋dp/dtmax、LVEDP、LVWI及TPR，增加SI及－dp/dtmax，亦能明显增加冠脉血流量，降低冠脉血管阻力，并明显降低心肌耗氧量、心肌氧提取率及心肌耗氧指数。结论：人参Rb组皂苷主要通过减少左室作功，降低心肌耗氧量，增加缺血心肌供血等环节发挥抗心肌缺血作用。     

Extracts from Astragalus membranaceus limit myocardial cell death and improve cardiac function in a rat model of myocardial ischemia

Ethnopharmacological relevance

The root of Astragalus membranaceus, known as “huang-qi”, is one of the most widely used Chinese herbal medicines for the prevention and treatment of myocardial ischemic diseases. However, the mechanisms governing its therapeutic effects are largely unknown.

Aims of the study

The aims of the present study were to investigate the cardioprotective effect of the root extract of Astragalu membranaceus (EAM) in myocardial ischemia and to explore its underlying mechanisms in ROS-mediated signaling cascade in vivo and in vitro.

Materials and methods

The saponins in EAM were analyzed using HPLC. The tests for the cardioprotective effects of EAM and its mechanisms were performed in vivo and in vitro. In vivo, the rat model of persistent myocardial ischemia was produced by occlusion of the left anterior descending (LAD) coronary artery. In vitro, the cardiomyocyte model of oxidative stress was mimicked by the direct free radical donor, H₂O₂.

Results

In vivo, the increased myocardial infarct size and the increased serum levels of lactate dehydrogenase (LDH), creatine kinase isoform MB (CK-MB), and cardiac troponin (cTnI) were significantly decreased by pre-treatment with EAM. Moreover, cardiac function, as assessed by±dP/dt, left ventricular developed pressure (LVDP), and left ventricular end-diastolic pressure (LVEDP), was dramatically improved. An oxidative stress biomarker, malondialdehyde (MDA), was reduced, and the antioxidant enzyme superoxide dismutase (SOD) was induced. In vitro, H₂O₂-triggered myocardial cell death and cytoplasm Ca²⁺ overload were blocked by treatment with EAM. Furthermore, the K_ATP channel blocker (5-HD, glibenclamide) blocked the anti-apoptotic protective effect of EAM on cardiomyocytes injured by H₂O₂.

Conclusions

The cardioprotection of EAM was manifested as a protection of tissue structure and as a decrease in serum markers of ischemic injury. The mechanisms underlying the EAM-mediated protective effects may involve improving cardiac function, attenuating the oxidative injury via a decrease in MDA, a maintenance in SOD, and a reduction in free radical-induced myocardial cell injury. Additionally, EAM enhanced the myocardial cell viability via arresting the influx of Ca²⁺ to block cell death and opening mitochondrial K_ATP channels to reduce cell apoptosis.     

电针心经腧穴对急性心肌缺血大鼠自主神经活动的影响

目的:观察电针心经"神门-通里"经脉段对急性心肌缺血大鼠交感神经和迷走神经放电的影响,探讨两者在电针心经改善急性心肌缺血中的协同调节作用。方法:SD大鼠随机分为伪手术组、模型组和电针心经组,每组10只。冠状动脉左前降支结扎法复制大鼠急性心肌缺血模型。电针心经组给予电针刺激大鼠心经"神门-通里"经脉段,刺激20min。用两根铂金丝电极分别同步引导左侧交感神经和迷走神经,同时记录模型复制前5min,结扎后即刻,电针后1、3、5、15 min的心电图、交感神经和迷走神经放电频率。结果:急性心肌缺血模型复制后,与伪手术组比较,模型组大鼠各时相心率、心电图J点电压、交感神经放电频率显著升高(P0.01),迷走神经放电频率显著降低(P0.01);与模型组比较,电针心经组大鼠各时相心率、心电图J点电压、交感神经放电频率均显著降低(P0.01),迷走神经放电频率显著升高(P0.01)。结论:电针心经可通过同时抑制交感神经放电和促进迷走神经放电,发挥改善急性心肌缺血的协同调节作用。     

Cardioprotective effect of water and ethanol extract of Salvia miltiorrhiza in an experimental model of myocardial infarction

Ethnopharmacological relevance

Salvia miltiorrhiza has long been used in the traditional Chinese formulations for the treatment of heart ischemic diseases.

Aim of the study

We investigated the cardioprotective effect of purified Salvia miltiorrhiza extract (SME) in an experimental model of acute myocardial infarction.

Materials and methods

Following induction of acute myocardial infarction in rats by adminstration of isoproterenol, hemodynamic and electrocardiographic parameters were monitored and recorded continuously, cardiac enzymes and parameters of oxidative stress were measured, and histopathological examination of heart tissue was performed. Experiments were performed in rats treated with SME or vehicle, as well as in those treated with Fufang Danshen Tablet (FDT) as a positive control which has previously been shown to prevent myocardial ischemia.

Results

Isoproterenol-treated rats showed reductions in left ventricular systolic pressure as well as in maximum and minimum rate of developed left ventricular pressure, together with an increase in left ventricular end-diastolic pressure. They also demonstrated ST-segment elevation, together with increases in serum levels of lactate dehydrogenase, glutamic oxalacetic transaminase, creatine kinase and malondialdehyde, as well as decreases in serum activities of glutathione peroxidase and superoxide dismutase. Oral administration of SME (29.76 or 59.52 mg/kg) blunted all of the hemodynamic and biochemical changes induced by isoproterenol, as did FDT (1210 mg/kg). The protective effect of SME on isoproterenol-induced myocardial damage was further confirmed by histopathological examination.

Conclusions

Our results suggest that SME affords protection against isoproterenol-induced myocardial infarction.     

Effect of the total saponins of Aralia elata (Miq) Seem on cardiac contractile function and intracellular calcium cycling regulation

Ethnopharmacological relevance

Total saponins of Aralia elata (Miq) Seem (AS) from the Chinese traditional herb Longya Aralia chinensis L. can improve cardiac function, although the active mechanism remains poorly understood. The present study aimed to determine the direct effect of AS on cardiac function in dogs and the effects on Ca²⁺ transient and contractions in isolated rat cardiomyocytes.

Material and Methods

In anesthetized dogs, hemodynamic indexes and myocardial oxygen consumption were determined before and after AS was administered. In isolated adult rat cardiomyocytes, contractile and intracellular Ca²⁺ properties were determined simultaneously in real time by using an IonOptix MyoCam system.

Results

Our results showed that AS directly induced a positive inotropic effect and improved coronary blood flow and energy metabolism, indicating that AS induced a beneficial effect to treat myocardial ischemia/reperfusion injury. Moreover, AS increased sarcomere shortening, maximal velocity of shortening/relengthening (±dL/dt), amplitude of [Ca²⁺]_i transients and SERCA activity in a concentration-dependent manner. PKCε was also activated after the cells were treated with AS.

Conclusion

These findings revealed the positive inotropic effect of AS on canine myocardium and isolated rat cardiomyocytes. This effect was possibly associated with an increase in amplitude of the [Ca²⁺]_i transient and PKCε-dependent signaling pathway.     

电针“神门”“太溪”穴对急性心肌缺血家兔心交感神经电活动的影响

目的:通过观察电针"神门""太溪"穴对急性心肌缺血家兔心交感神经电活动的影响,研究电针同名经穴对急性心肌缺血作用的相对特异性。方法:随机选择8只家兔作为正常组,余家兔经股静脉注射垂体后叶素3 U/kg复制急性心肌缺血模型。将模型复制成功的家兔随机分为模型组、"神门"组、"太溪"组和非经穴组,每组8只。各电针组刺激电流为1.1 mA,频率为2 Hz,每次刺激10 min,进行电针治疗。采用BIOPAC生物信号采集系统观察各组家兔30 min内心率和交感神经活动变化情况。结果:急性心肌缺血模型复制后,心率明显下降、心交感神经电活动的频率一过性增多后急剧减少,与正常组家兔比较差异有统计学意义(P0.01)。在停针即刻,"神门"组家兔的心率和心交感神经电活动的频率与模型组比较显著增高(P0.01);"太溪"组及非经穴组家兔心率和心交感神经电活动的频率与模型组比较差异无统计学意义(P0.05),与正常组比较显著降低(P0.01)。在20 min时刻,"神门"组家兔的心交感神经电活动频率高于模型组(P0.01),与正常组家兔比较差异无统计学意义(P0.05);"太溪"组与非经穴组家兔的心交感神经电活动频率与模型组比较差异无统计学意义(P0.05),与正常组比较显著下降(P0.01)。结论:电针不同经穴对急性心肌缺血家兔的调整作用存在一定的相对特异性,电针心经原穴"神门"的调整效应优于其同名经原穴"太溪"。     

电针内关、心俞及关元俞对急性心肌缺血兔心功能的影响

目的：探讨电针内关、心俞、关元俞对急性心肌缺血兔心功能的影响。方法36只兔按随机数字表法分为对照组、模型组和治疗组,每组12只。经颈静脉注射垂体后叶素制作兔急性心肌缺血模型,分别于造模前10 min、造模后1 h及治疗后1周检测心肌组织丙二醛（MDA）、血清肌酸激酶（CK）浓度,并通过检测各组左心室内压最大上升速率（dp/dtmax）和左心室内压力峰值（LVSP）评价心功能。结果电针治疗1周后,治疗组CK、MDA浓度降低[分别为（120.21±10.67）IU/L、（21.35±2.04）mmol/L],与模型组[分别为（162.37±13.21）U/L、（30.13±2.75）mmol/L]比较差异有统计学意义（P 均＜0.05）;dp/dtmax和 LVSP 下降率[分别为（20.0±2.43）%、（7.22±0.97）%]较模型组[分别为（31.5±4.14）%、（12.19±2.21）%]降低（P均＜0.05）。结论电针内关、心俞、关元俞配穴可改善兔急性心肌缺血后心功能,对兔急性心肌缺血有保护作用。     

当归红芪多糖对急性心肌缺血大鼠的保护作用

目的:观察当归红芪多糖对急性心肌缺血大鼠的保护作用,并探讨其相关的作用机制。方法:将80只雄性Wistar大鼠随机分为假手术组(SH),缺血组(MI),当归红芪多糖3 g·kg-1组(LD),当归红芪多糖6 g·kg-1组(MD),当归红芪多糖12 g·kg-1组(HD),每组16只。通过结扎大鼠左冠状动脉前降支建立急性心肌缺血模型;缺血+当归红芪多糖干预组分别于缺血24 h时用当归红芪多糖3,6,12 g·kg-1ig,各组动物分别于治疗后36 h及14 d时取材。应用生化分析仪测定大鼠血清肌酸激酶(CK),肌酸激酶同工酶(CK-MB),乳酸盐脱氢酶(LDH),乳酸盐脱氢酶同工酶(LDHI)含量;采用逆转录-聚合酶链式反应(RT-PCR)技术检测大鼠心肌组织热休克蛋白70(Hsp70),Hsp32,血管内皮生长因子(VEGF)mRNA的表达变化情况。结果:与SH组比较,MI组ST段均抬高(P0.05);与SH组比较,MI组CK,CK-MB,LDH,LDHI含量在36 h时有显著升高,Hsp70,Hsp32,VEGF mRNA表达量增加(P0.05,P0.01);与MI组比较,当归红芪多糖各剂量组CK,CK-MB,LDH,LDHI含量在36 h时明显升高,Hsp70,Hsp32,VEGF mRNA表达增高(P0.05,P0.01)。结论:当归红芪超滤物对急性心肌缺血大鼠具有明显的保护作用。     

Panax notoginseng saponins inhibit ischemia-induced apoptosis by activating PI3K/Akt pathway in cardiomyocytes

Aim of this study

The panax notoginseng saponins (PNS) have been clinically used for the treatment of cardiovascular diseases and stroke in China. Evidences demonstrated that PNS could protect cardiomyocytes from injury induced by ischemia, but the underlying molecular mechanisms of this protective effect are still unclear. This study was aimed to investigate the protective effect and potential molecular mechanisms of PNS on apoptosis in H9c2 cells in vitro and rat myocardial ischemia injury model in vivo.

Materials and methods

H9c2 cells subjected to serum, glucose and oxygen deprivation (SGOD) were used as in vitro models and SD rats subjected to left anterior descending (LAD) coronary artery ligation were used as in vivo models. The anti-apoptotic effect of PNS was evaluated by Annexin V/PI analysis or TUNEL assay. Mitochondrial membrane potential (Δψm) was detected by JC-1 analysis. The expression of Akt and phosphorylated Akt (p-Akt) were detected by western blot assay.

Results

PNS exhibited anti-apoptotic effect both in H9c2 cells and in ischemic myocardial tissues. However, the effect was blocked in vitro by LY294002, a specific PI3K inhibitor. The anti-apoptotic effect of PNS was mediated by stabilizing Δψm in H9c2 cells. Furthermore the indices of the left ventricular ejection fractions (EF), left ventricular fractional shortening (FS), left ventricular dimensions at end diastole (LVDd) and left ventricular dimensions at end systole (LVDs) suggested that PNS improved rats cardiac function. PNS significantly increased p-Akt both in H9c2 cells and in ischemic myocardial tissues and this effect was also blocked by LY294002 in H9c2 cells.

Conclusion

Results of this study suggested that PNS could protect myocardial cells from apoptosis induced by ischemia in both the in vitro and in vivo models through activating PI3K/Akt signaling pathway.     

山楂叶总黄酮对心肌缺血再灌注损伤大鼠心功能的影响

 目的观察山楂叶总黄酮(hawthornleavesflavonoids,HLF)对心肌缺血再灌注损伤大鼠的心功能保护作用。方法在结扎大鼠冠状动脉左前降支30min再灌注120min造成心肌缺血再灌注损伤模型,观察HLF对大鼠心功能、心肌酶学和脂质过氧化的影响。结果HLF能够对抗心肌缺血再灌注引起的左心室内压(LVSP)、左心室内压最大上升与下降速率(±dp/dtmax)、动脉血压的下降,并能够使心肌组织Na⁺-K⁺-ATP酶活性及丙二醛(MDA)含量降低和SOD的含量增高。结论HLF对大鼠心肌缺血再灌注引起的心功能减弱具有明显的保护作用,其机制可能与改善能量代谢障碍和抑制自由基生成或清除氧自由基作用有关。     

Protective effects of cinnamic acid and cinnamic aldehyde on isoproterenol-induced acute myocardial ischemia in rats

Ethnopharmacological relevance

Cinnamomum cassia is a well-known traditional Chinese herb that is widely used for the treatment of ischemic heart disease (IHD). It has favorable effects, but its mechanism is not clear. To investigate the effects of cinnamic aldehyde (CA) and cinnamic acid (CD) isolated from Cinnamomum cassia against myocardial ischemia produced in rats by isoproterenol (ISO).

Materials and methods

Ninety male Sprague-Dawley rats were randomized equally to nine groups: a control group, an untreated model group, CA (22.5, 45, 90 mg/kg) or CD (37.5, 75, 150 mg/kg) treatment, or propranolol (30 mg/kg). Rats were treated for 14 days and then given ISO, 4 mg/kg for 2 consecutive days by subcutaneous injection. ST-segment elevation was measured after the last administration. Serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), and blood rheology were measured after the rats were sacrificed. The hearts were excised for determining heart weight index, microscopic examination, superoxide dismutase (SOD) and malondialdehyde (MDA) measurements.

Results

CA and CD decreased the ST elevation induced by acute myocardial ischemia, decreased serum levels of CK-MB, LDH, TNF-α and IL-6, and increased serum NO activity. CA and CD increased SOD activity and decreased MDA content in myocardial tissue.

Conclusion

CA and CD were cardioprotective in a rat model of ischemic myocardial injury. The protection was attributable to anti-oxidative and anti-inflammatory properties, as well as increased NO. The results support further study of CA and CD as potential treatments for ischemic heart disease.     

丹蒌片对大鼠心肌缺血再灌注损伤的保护作用及机制

目的:观察丹蒌片对大鼠心肌缺血再灌注损伤(MIRI)的保护作用,并探讨其机制。方法:将80只健康成年雄性Wistar大鼠随机分为假手术组(以0.5%羧甲基纤维素钠溶液10 m L·kg~(-1)灌胃)、模型组(以0.5%羧甲基纤维素钠溶液10m L·kg~(-1)灌胃)、丹蒌片组(0.9 g·kg~(-1))。预防性给药7 d后,结扎大鼠心脏冠脉左前降支,50 min后复灌,制作大鼠心肌缺血再灌注损伤模型。每组取6只大鼠于复灌2 h检测血清乳酸脱氢酶(LDH),肌酸激酶同工酶(CK-MB),内皮素(ET),一氧化氮(NO)水平及心肌组织丙二醛(MDA)及髓过氧化物酶(MPO)水平。剩余大鼠于造模前及复灌48 h进行心脏射血分数检测,每组取6只进行原位末端转移酶标记技术(TUNEL)染色评估心肌细胞凋亡指数,蛋白免疫印迹法(Western blot)检测心肌含半胱氨酸的天冬氨酸蛋白水解酶(Caspase)-3,B细胞淋巴瘤-2(Bcl-2)及Bcl-2相关X蛋白(Bax)蛋白表达。余大鼠行依文思蓝-TTC染色评估心肌梗死面积。结果:复灌2 h时,与模型组比较,丹蒌片组血清LDH及CK-MB均明显降低(P0.05),血清ET-1明显降低,NO明显升高(P0.05),心肌组织MDA及MPO明显升高(P0.05)。复灌48 h时,与模型组比较,丹蒌片组心脏EF值明显上升(P0.05),心肌梗死范围明显下降(P0.05),心肌凋亡指数明显下降(P0.01);与模型组比较,丹蒌片组心肌Caspase-3,Bax蛋白表达明显升高(P0.05,P0.01),Bcl-2蛋白表达下降(P0.05)。结论:丹蒌片在MIRI早期可以保护内皮细胞功能、抑制氧化及炎症浸润,在MIRI晚期可能通过抑制细胞凋亡,缩小心肌梗死面积,改善心功能来实现对心脏的保护作用。     

Protective effects of muscone on ischemia-reperfusion injury in cardiac myocytes

Ethnopharmacological relevance

Musk has been traditionally used in Chinese medicine as the main ingredient of many formulations for the treatment of chest pain and angina pectoris.

Aim of the study

To investigate the protective effects of muscone (the active ingredient of musk) on ischemia-reperfusion (I/R) injury induced by hypoxia and low glucose in primary cultured rat cardiac myocytes.

Materials and methods

Primary cultures of neonatal rat cardiac myocytes were subjected to ischemia-reperfusion in media, with or without muscone. Cell viability, release of lactic acid dehydrogenase (LDH), superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, creatine kinase (CK) and caspase-3 activities, as well as intracellular free Ca²⁺ concentrations, were measured. Cellular apoptosis and mitochondrial membrane potential (MMP) were assessed by flow cytometry, and the expression of Bcl-2 and Bax proteins was assessed by Western blotting.

Results

Following the exposure of cardiac myocytes to ischemia-reperfusion, there was a marked decrease in pulsating frequency, cell viability, SOD activity, MMP, and the expression of Bcl-2 protein, accompanied by increased LDH release, MDA production, CK and caspase-3 activities, intracellular free Ca²⁺ concentrations, rate of apoptosis, and expression of Bax protein. Pretreatment with muscone (0.215, 0.43, 0.86 μg/mL) prior to I/R injury significantly attenuated the above changes.

Conclusion

Muscone has a protective effect against I/R injury in cardiac myocytes, indicating that muscone may potentially provide therapeutic benefit in I/R injury by inhibiting cellular oxidative stress and apoptosis.     

芪丹通脉片对大鼠心肌细胞Ca2+及超微结构的影响

目的探讨芪丹通脉片(QDTM T)对急性心肌缺血的防治作用。方法SD大鼠ig QDTM T(2 g/kg)两周后,sc异丙肾上腺素(Iso,5 m g/kg)诱导急性心肌缺血模型。通过透射电镜观察心肌超微结构的变化;用比色法测定心肌组织及心肌细胞线粒体中C a2 水平及心肌细胞线粒体中C a2 -ATPase活力的变化。结果大鼠igQDTM T两周后,sc Iso所造成的心肌超微结构的损害明显减轻;心肌细胞线粒体中C a2 -ATPase活力增加,而心肌组织及心肌细胞线粒体中C a2 水平显著降低(P<0.01)。结论QDTM T可能是通过抑制心肌细胞线粒体中钙超载及保护心肌细胞超微结构,达到防治急性心肌缺血的目的。     

精制血府胶囊对犬急性心肌缺血心脏血流动力学和心肌耗氧量的影响

目的：探讨精制血府胶囊对犬急性心肌缺血心脏血流动力学和心肌耗氧量的作用机理。方法：采用结扎犬冠状动脉的方法造成急性心肌缺血模型，十二指肠给药，观察其对缺血心脏冠状动脉血流量、心输出量及心脏收缩舒张功能等的影响。结果：结扎犬冠状动脉造成急性心肌缺血后，空白对照组心脏收缩舒张功能减退、冠状动脉血流量及心输出量降低，而精制血府胶囊组各项指标均有一定改善，大剂量组更为显著，并可降低心肌耗氧量。结论：精制血府胶囊可保护火急性心肌缺血心脏的泵血功能，其机理可能与降低心肌耗氧量、增加心肌供血有关。