复方丹参注射液对离体蟾蜍心功能影响及机制的研究

目的 观察复方丹参注射液（Compound Danshen Injection,CDI）对离体蛙心心率和心肌收缩力的影响.方法 根据斯氏蛙心插管方法,用不同浓度的CDI对离体蛙心进行灌流,采用BL-420生物机能实验系统记录心率和心肌收缩力的变化.结果 CDI在一定浓度范围内能增强心肌收缩力（P＜0.05）,0.05mg/ml增强心肌收缩力较显著;CDI在一定浓度范围内可降低心率,以0.025 mg/ml降低心率最明显（P＜0.05）;CDI可对抗维拉帕米对心肌的负性作用,差异具有统计学意义（P＜0.05）.结论 CDI在一定浓度范围内可降低离体蛙心心率、增强心肌收缩力,其机制可能与促进钙离子内流有关.     

葛根注射液抗心肌缺血的药理作用研究

目的 考察葛根注射液的抗心肌缺血作用.方法 考察葛根注射液高中低剂量组对大鼠离体心脏左室峰压(LVSP)、冠脉流量(CF)及大鼠离体心脏缺血再灌注后的LVSP、左室舒张期末压(LVEDP)、心率(HR)、CF的影响.结果 葛根注射液可升高大鼠离体心脏心肌收缩力及冠脉流量;对离体心脏缺血再灌注导致的LVSP和LVEDP的升高、心率及冠脉流量的降低均有对抗作用.结论 葛根注射液具有抗心肌缺血的作用.     

葛根注射液抗心肌缺血作用药理研究

目的 考察葛根注射液的抗心肌缺血作用。方法 考察葛根注射液高中低剂量组对大鼠离体心脏左室峰压(LVSP)、冠脉流量(CF)及大鼠离体心脏缺血再灌注后的LVSP、左室舒张期末压(LVEDP)、心率(HR)、CF的影响。结果 葛根注射液可升高大鼠离体心脏心肌收缩力及冠脉流量;对离体心脏缺血再灌注导致的LVSP和LVEDP的升高、心率及冠脉流量的降低均有对抗作用。结论 葛根注射液具有抗心肌缺血的作用。     

常用动物实验麻醉药对离体蟾蜍心脏作用的比较

目的：观察氯胺酮、水合氯醛、氨基甲酸乙酯与戊巴比妥钠对离体蟾蜍心脏作用。方法：选用氯胺酮（40mg/kg）、水合氯醛（400mg/kg）、氨基甲酸乙酯（2000mg/kg）、戊巴比妥钠（40mg/kg）分别作用于离体蟾蜍心脏,观察不同实验动物麻醉药对离体蟾蜍心脏心率及心肌收缩力的影响。结果：组内比较时四种麻醉药均对心率有明显的抑制作用（P〈0.05）,且氨基甲酸乙酯具有显著统计学意义（P〈0.01）;四种麻醉药均对心肌收缩力有明显的抑制作用（P〈0.05）,且氯胺酮和戊巴比妥钠具有显著统计学意义（P〈0.01）。结论：四种实验动物麻醉药对离体蟾蜍心脏均有抑制作用,以氨基甲酸乙酯的心脏影响最大。     

大蒜素对蟾蜍离体心脏功能影响机制的探究

目的探究大蒜素对蟾蜍离体心脏功能的影响及其影响机制。方法采用斯氏离体蛙心灌流观察不同浓度的大蒜素溶液和普萘洛尔对蟾蜍离体心脏功能的影响。结果 0.0005 mg/mL、0.00275 mg/mL和0.005 mg/mL的大蒜素使心肌收缩加强,且随浓度增加而作用增强,但对心率影响不大;加普萘洛尔后,0.005 mg/mL大蒜素溶液对心肌收缩幅度无明显影响。结论大蒜素使蟾蜍离体心脏的心肌收缩力加强,但对心率作用不明显;大蒜素液对心肌收缩的加强作用,可被普萘洛尔所抑制。     

氧化苦参碱的强心作用

用多种实验动物研究了氧化苦参碱的强心作用,结果表明:氧化苦参碱(05、5、50mol/L)能明显增加正常离体蟾蜍心肌收缩力、心输出量,强心同时不增加心率;显著增加戊巴比妥钠和低钙离体心衰模型的心肌收缩力、心输出量(P<005或P<001);50mmol/L可使心肌收缩力、心输出量完全恢复到心衰前水平,对心率无明显影响;能不同程度地加强离体豚鼠、大鼠、兔乳头肌的收缩力,均呈现良好的量效关系,对豚鼠乳头肌更为敏感;增加大鼠离体右心房心肌收缩力同时降低其自发收缩频率(P<001).     

麦冬有效成份的药理研究

用八本-Hartung 法离体蟾蜍心脏灌流证明,麦冬皂甙明显增强离体蟾蜍心脏的心肌收缩力及增加心输出量。Langendorff 法豚鼠离体心脏灌流表明,麦冬总皂甙及总氨基酸小剂量均可使心肌收缩力增强,冠脉流量增加,大剂量则抑制心肌,减少冠脉流量,但二者对心率无甚影响。小鼠游泳试验表明麦冬氨基酸具明显的抗疲劳作用,麦冬多糖也具有一定抗疲劳作用。此外,麦冬总氨基酸还对阈下催眠量的戊巴比妥钠具有协同作用。     

乌榄叶水提取物对大鼠离体心脏灌流的作用探究

目的探究乌榄叶水提取物对大鼠离体心脏的冠脉流量、心肌收缩力及心率的影响。方法采用Langendorff离体心脏灌流法,通过MedLab生物信号采集处理系统,观察药物对正常大鼠离体心脏的冠脉流量、心肌收缩力及心率的作用。结果乌榄叶水提取物对大鼠冠脉流量作用效果与丹参的类似,与生理盐水空白组比较差异有统计学意义,具有稳定和增加冠脉流量作用,给药后前6 min表现为加强心肌收缩力作用,而后均逐渐减弱恢复。心率在整个过程中持续下降,且下降速率快。结论乌榄叶水提取物对冠脉流量和心肌收缩力具有先增加后减少至给药前状态的双向作用,并有较快、较强的慢心率作用。结果提示乌榄叶可能有利于降低心脏耗氧量,维持心功能,起保护心肌的作用。     

沙棘总黄酮对离体心脏的抗心律失常作用

沙棘总黄酮(TFH)对离体大鼠心脏可显著延长缺氧性心律失常出现时间,提高室颤阈值,延缓房室传导,减慢心率,减弱心肌收缩力和对抗由缺氧引起的心率减慢及心肌收缩力减弱的作用。TFH可轻度延长离体豚鼠左房功能不应期,明显对抗乌头碱诱发离体豚鼠右房节律失常的作用。     

赤土茯苓苷对离体大鼠心脏缺血再灌注损伤的保护作用

采用 Langendorff离体大鼠非循环灌流模型测定赤土茯苓苷对离体大鼠缺血再灌注损伤时心肌收缩力、冠脉阻力、心率的影响及其抗脂质过氧化作用。结果 2 mg/L,1 0 mg/L,50 mg/L赤土茯苓苷可保护缺血再灌注心肌超氧化物歧化酶与硒谷胱甘肽过氧化物酶 ,降低脂质过氧化产物丙二醛的含量 ,能增加再灌后冠脉流量、冠脉阻力 ,促进心肌收缩幅度的恢复 ,减轻心脏水肿 ,但对心率的影响未见统计学差异     

Calcium interferes with the cardiodepressive effects of beta-blocker overdose in isolated rat hearts

Propranolol, timolol and sotalol were compared with respect to their cardiotoxic properties in isolated, spontaneously beating rat hearts. Propranolol and timolol induced a dose-dependent decrease in myocardial contractility. A high dose of sotalol had only modest negative inotropic effects. Similar reductions in myocardial contractility were observed in isolated, ventricle-stimulated rat hearts. These observations were similar to those in a previous study in which spontaneously beating and ventricle-stimulated reserpinized rat hearts were investigated. Spontaneously beating rat hearts were perfused with a high-, a normal- and a low-Ca++ medium, each with and without propranolol, timolol and sotalol. Addition of each beta-blocker to a normal-Ca++ medium induced a decrease of myocardial contractility and of heart rate and an increase of AV-conduction time when compared with the drug-free medium. In a high-Ca++ medium containing the same concentration of each beta-blocker, a less pronounced decrease of myocardial contractility was observed. Heart rate decreased and AV-conduction time increased to the same extent as after perfusion with the drug containing normal-Ca++ medium. With respect to the corresponding drug-free medium perfusion with a low-Ca++ medium with each beta-blocker enhanced the decline in myocardial contractility, most pronounced in propranolol and timolol containing media. For propranolol and sotalol the decrease in heart rate and increase in AV-conduction time were similar to the results after administration of the same beta-blocker in a high- and a normal-Ca++ perfusion media. Timolol caused an electromechanical dissociation. It was concluded that in beta-blocker intoxication the negative-inotropic phenomena cannot be explained by an action of the drugs on the beta-receptor since the results in reserpinized and non-reserpinized rat hearts were similar. Other effects have to be responsible for the observed cardiotoxic phenomena. The present results indicate that these phenomena can be influenced by Ca++ and or can be attributed to differences in lipophilicity.     

Cardiotropic activity of total bufadienolides from the poison of Central Asian toad Bufo viridis

The sum of bufadienolides (bacagin) isolated from the poison of Bufo viridis toad occurring in Central Asia produces a selective strophanthin-K-like action upon the heart function, increasing myocardial contractility, retarding cardiac rhythm, and positively influencing the parameters of myocardial metabolism. The mechanism of realization of the positive ionotropic effect of bacagin is probably related to the ability of increasing the basal level of cytosol calcium at the expense of inhibiting the activity of Na+/K(+)-ATPase and, to some extent, Ca(2+)-ATPase in endoplasmic reticulum.     

尼可刹米对离体蟾蜍心室肌收缩性及电活动的影响

目的:观察尼可刹米对蟾蜍心室肌收缩性及电活动的影响.方法:成年健康蟾蜍20只,体质量80～100g,雌雄不限,机分成对照组和尼可刹米组,每组10只.制备改良蛙心灌流动物模型,同步描记离体心脏收缩曲线和心室肌电活动.对照组蛙心插管内加入正常任氏液,记录60 min内蛙心的跳动和电活动;尼可刹米组在蛙心插管内依次加入含0、0.25、0.5、1、2 mg/L尼可刹米的任氏液,记录不同浓度的尼可刹米对蟾蜍心室肌收缩幅度和电活动的影响.结果:尼可刹米在0.5～2 mg/L范围内可以增加蟾蜍心室肌收缩幅度和放电幅度.结论:尼可刹米可增加蟾蜍心室肌收缩性和电活动.     

PTEN inhibitors cause a negative inotropic and chronotropic effect in mice

Inactivation of phosphatase and tensin homologue deleted on chromosome ten (PTEN) decreases cardiac contractility under basal conditions and induces cardioprotection against ischemia–reperfusion injury. However, the pharmacological effect of PTEN inhibitors on cardiac contractility has not been studied before. In the present study, we investigated the hypothesis that PTEN inhibition decreases cardiac contractility in mice. We first exposed isolated mouse hearts to the PTEN inhibitor bpV(phen) (40 μM), the phosphoinositide-3 kinase inhibitor wortmannin (1 μM), and the PTEN-resistant PIP3 analog 3-phosphorothioate-PtdIns(3,4,5)P3 (3-PT-PTP, 0.5 μM) for 10 min. Left ventricular pressure was measured by a Mikro-tip pressure catheter. We then inhibited PTEN in mice by intra-peritoneal injection of VO-OHpic (10 μg/kg) 30 min before ischemia and then exposed them to 30 min of ischemia and 120 min of reperfusion. At the end of the experiments, hearts were isolated for measurement of myocardial infarct size by 1.5% triphenyltetrazolium chloride. Left ventricular systolic pressure and heart rate were significantly decreased by bpV(phen). Consistent with the result, the maximal rate of left ventricular pressure increase or decrease was significantly decreased by bpV(phen). 3-PT-PIP3 mimicked the effect of bpV(phen), and the opposite effect on cardiac contractility was seen with wortmannin. Moreover, inhibition of PTEN in vivo by VO-OHpic decreased left ventricular systolic pressure and heart rate before ischemia, but resulted in an increase in cardiac functional recovery and a decrease in myocardial infarct size after ischemia–reperfusion. In conclusion, PTEN inhibition causes a negative inotropic and chronotropic effect while inducing cardioprotection against ischemia–reperfusion injury.     

Dipyridamole induced myocardial recovery after global ischemia.

1. An experimental comparative study on isolated guinea pig hearts was carried out to determine the effect of dipyridamole added to the reperfusion solution on myocardial recovery after global ischemia. 2. After 20 min of normothermic ischemia two groups of solutions: (1) Krebs solution; (2) Krebs + dipyridamole 20 micrograms/l (10 experiments in each group) were used for reperfusion. 3. Postischemic myocardial functions (heart rate, ventricular contractility, heart work) and tissue enzymes (CPK-MB, LDH) were compared with their preischemic values. 4. Addition of dipyridamole 20 micrograms/l to reperfusion solution improved postischemic myocardial functions and decreased myocardial injury.     

In vitro cardiotoxicity and mechanism of action of the Egyptian green toad Bufo viridis skin secretions

Amphibian skin secretions are considered a rich source of biologically active compounds and are known to be rich in bufadienolides, peptides and alkaloids. Bufadienolides are cardioactive steroids derived from animals and plants as well. The current study was conducted to investigate the influence of skin secretions of the Egyptian green toad Bufo viridis (SSBV) on the cardiac electrical activity. Isolated toad’s heart was used to reveal the mechanism of action. Application of SSBV (40 μg/ml) into isolated toad’s heart significantly decreased the heart rate (HR) accompanied by an elongation in the conduction time (P–R interval). A pronounced increase of the ventricular contraction (R-wave amplitude) was observed after SSBV application. Marked electrocardiographic changes were induced within minutes (5–20 min) of SSBV perfusion of the isolated hearts; such as sinus arrhythmias, junctional ectopic beats, negative QRS deflection, ventricular tachycardia and heart block. The mechanism of action of SSBV was studied by direct application of different autonomic and ion channels antagonists (atropine sulphate, propranolol and verapamil) to isolated toad’s heart. Neither atropine nor verapamil could attenuate the noticed negative chronotropic and positive inotropic effects. Meanwhile, post-treatment with propranolol decreased R-wave amplitude. Taken together, it can be concluded that: (i) SSBV has a negative chronotropic, dromotropic and positive inotropic effects on isolated toad’s heart; (ii) the reported effects of SSBV could be due to inhibition of Na⁺–K⁺ ATPase and through ß-adrenergic receptors.     

参麦注射液渗透压和溶血率现状的调查

目的：为做好参麦注射液安全性再评价工作提供数据参考。方法：渗透压测定采用冰点测定法,对样品原液及其稀释液进行渗透压测定,并计算与氯化钠注射液渗透压的比值;溶血率测定采用分光光度法,对样品原液及其稀释液进行溶血率测定。结果：渗透压测定,样品原液均为低渗溶液,渗透压值在96～180mOsmol/kg,1→4～1→8稀释后与氯化钠注射液渗透压比可达0.9;溶血率测定,样品稀释倍数在小于1→16时,样品均存在不同程度的溶血（溶血率〉5%）,1→32倍稀释时,溶血率均小于等于5%。结论：不同厂家生产的参麦注射液的渗透压和溶血率均存在一定的差异,建议增加渗透压和溶血率测定来控制其质量。     

Effect of sodium nitroprusside on myocardial performance and venous tone.

The action of sodium nitroprusside upon the mechanical performance of the isolated, working rat heart and on isolated bull veins has been studied. Cumulative concentrations of 1--1000 ng sodium nitroprusside per ml had no effect on left ventricular pressure, end-diastolic left ventricular pressure, dp/dtmax, cardiac output and calculated wall stiffness of isolated rat hearts with constant rate, preload and afterload. Isolated strips of bull veins contracted with noradrenaline showed a dose dependent relaxation by sodium nitroprusside in concentrations of 5--1000 ng per ml. This study shows that sodium nitroprusside has no direct effect on myocardial contractility and causes venous relaxation.     

Effect of ATP and verapamil as cardioplegic additives in the isolated guinea pig heart.

1. A comparative study on isolated guinea pig hearts was carried out to determine the effects of ATP and verapamil as cardioplegic additives. 2. The hearts were arrested by one of the plegic solutions: I, potassium 20 mmol/l; II, potassium 20 mmol/l+verapamil 1.1 mumol/l; III, potassium 20 mmol/l+ATP 10 mmol/l. After 45 min of hypothermic ischemia, the hearts were reperfused by Krebs-Henseleit buffer. 3. Postischemic percentage change of myocardial functions (heart rate, contractility, heart work) and tissue enzymes (LDH, SGOT, SGPT) were compared between the groups. 4. Although a rapid cardiac arrest could be obtained by verapamil added cardioplegia. Postischemic myocardial recovery was much better with ATP added cardioplegic solutions.