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。     

三七绒根提取物(76017)对心血管的作用

三七绒根提取物(76017)为三七绒根乙醇提出物的有效成分,毒性较低,给小白鼠静注LD_(50)为836±17mg/kg。 给麻醉猫静注76017 25～50 mg/kg,3～5分钟内冠脉流量最高增加79％(P<0.05),血压呈暂时性下降,心率也略减慢,心肌耗氧量减少,比给药前平均降低24.3％(P<0.05)。 在家兔离体心脏灌流实验中,当2％76017 0.1和0.2ml注入灌流系统时,小剂量组给药后1分钟,冠脉流量平均增加17.5％;大剂量组给药后5分钟和7.5分钟分别增加48％和43％,(P<0.05),心率也稍减慢(P>0.05)。小剂量组心肌收缩振幅在5分钟内最高增加48％(P<0.05)。 在家兔离体器官血管灌流的实验中,当2％76017 0.1和0.2ml注入灌流系统,记录5分钟内的峰值,小剂量组兔肾、耳及后肢的流量分别增加50,57和32％;而大剂量组分别增加70,64和33％。     

健心合剂对离体大鼠心脏冠脉流量及小鼠耳廓微循环的影响

目的:观察健心合剂对离体大鼠心脏冠脉流量及小鼠耳廓微循环的影响。方法:采用L angendorf法对大鼠离体心脏进行恒温恒压冠脉灌流,测定给药前、后冠脉流量及心肌收缩幅度、心率等变化,观察比较药物对冠脉血管的扩张作用及对心肌收缩幅度,心率的影响,以小鼠耳廓微循环的变化直接观测用药前后微循环的改变情况。结果:健心合剂能显著地增加大鼠心脏冠脉流量及心肌收缩幅度,减慢心率。使小鼠耳廓细动脉、细静脉的口径增大,毛细血管开放量增加。结论:健心合剂能增加冠脉流量,减慢心率,使心肌收缩幅度增加,改善微循环。     

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     

三七绒根提取物(76017)对心血管的作用

三七绒根提取物(76017)为三七绒根乙醇提出物的有效成分,毒性较低,给小白鼠静注LD₅₀为836±17mg/kg。给麻醉猫静注76017 25～50 mg/kg,3～5分钟内冠脉流量最高增加79%(P<0.05),血压呈暂时性下降,心率也略减慢,心肌耗氧量减少,比给药前平均降低24.3%(P<0.05)。在家兔离体心脏灌流实验中,当2%76017 0.1和0.2ml注入灌流系统时,小剂量组给药后1分钟,冠脉流量平均增加17.5%;大剂量组给药后5分钟和7.5分钟分别增加48%和43%,(P<0.05),心率也稍减慢(P>0.05)。小剂量组心肌收缩振幅在5分钟内最高增加48%(P<0.05)。在家兔离体器官血管灌流的实验中,当2%76017 0.1和0.2ml注入灌流系统,记录5分钟内的峰值,小剂量组兔肾、耳及后肢的流量分别增加50,57和32%;而大剂量组分别增加70,64和33%。     

三七的药理作用研究

<正> 三七别名田七,为五加科人参属植物Panax notoginseng(Burk)F.H.Chen的根茎,是常用中药之一。其功能为滋补强壮、止血化瘀、消肿止痛,治疗血虚、跌打损伤、崩漏内出血、咳血、便血等。近年来临床用于治疗冠心病、脑血管意外后遗症、肝炎等症有效。本文仅从三七药理作用方面综述如下: 对心血管系统的作用对心脏血液动力学的影响苏雅等报道用三七根提取液(乙醇提取)给麻醉猫iv 25-50mg/kg,血压暂时性压低,心肌耗氧量降低,冠脉流量明显增加。将三七根提取液按1∶20000浓度加入灌流液中,能增加离体豚鼠心脏冠脉流量84.04%,同时心肌收缩力也增强.经十二指肠给予三七提取物100mg/kg,冠脉流量增加57.03%,并能持续3h以上,其作用与给予潘生丁2mg/kg的结果相似。蔡锡林等发现三七冠心     

淫羊藿治疗冠心病的研究 5.淫羊藿对心血管系统的药理作用

本文研究了淫羊藿煎膏溶液及其5-1-1提取液对冠脉流量、心肌缺血的作用,对心肌收缩力、耗氧量的影响,对血压及外周阻力的影响。结果(1)20%煎膏溶液使离体豚鼠心脏冠脉流量平均增加132.1%,100%5-H 提取液1ml/kg 使麻醉狗冠脉流量平均增加112.2%,阻力下降30%;100%5-1-1提取液0.075ml/只可使小白鼠心肌摄取 Rb~(86)量增加50%。(2)100%5-1-1提取液8ml/kg 使大鼠用垂体后叶素诱发心肌缺血60%受到保护。(3)100%水煎膏0.5ml/kg,使在位兔心收缩力下降52.2%。(4)煎膏液对大鼠心肌匀浆耗氧量无明显影响。(5)100%煎膏溶液0.5ml/kg 使麻醉兔血压平均下降20%,外周阻力下降50%。     

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。     

黄芪注射液对离体大鼠心脏功能及Na+-K+-交换ATP酶活性的影响

目的：观察黄芪注射液对离体心脏的影响。方法：采用大鼠离体心脏,以Ｋｒｅｂｓ＿Ｈｅｎｓｅｌｅｉｔ 灌流液进行离体灌流。观察给黄芪注射液灌流前及灌流后５ ,１０ ,１５ ,２０ 及３０ ｍｉｎ 心肌收缩幅度、冠状动脉（ 冠脉） 流量及心率等指标。试验结束后取部分左心室心肌,以比色法测定心肌细胞膜Ｎａ＋＿Ｋ＋＿交换ＡＴＰ酶活性。结果：给药后５ ～３０ ｍｉｎ ,２０ ｍｇ／Ｌ,１００ｍｇ／Ｌ 及５００ ｍｇ／Ｌ３ 个剂量组黄芪注射液均有显著增加冠脉流量的作用,同时,心肌收缩幅度亦明显增加,与对照组比较差异均有显著意义（ Ｐ＜ ０ ．０５ 或Ｐ＜ ０ ．０１） ;５００ ｍｇ／Ｌ组给药后５ 及１５ ｍｉｎ 心率明显增加;５００ ｍｇ／Ｌ 及１００ ｍｇ／Ｌ 剂量组心脏心肌组织Ｎａ＋＿Ｋ＋＿交换ＡＴＰ 酶活性明显提高,与对照组比较差异有非常显著意义（ Ｐ＜ ０ ．０１） 。结论：黄芪注射液能够明显增加正常离体大鼠心脏冠脉流量、心肌收缩幅度及心率,并有增加心肌细胞膜Ｎａ＋＿Ｋ＋＿交换ＡＴＰ 酶活性的作用。     

灵芝对冠脉循环影响的实验研究

赤灵芝发酵总硷从犬的股静脉注射之后,冠脉血流明显增加(62%),冠脉血管阻力和心肌耗氧量下降。实验证明,灵芝能改变冠脉血流动力和心肌代谢。发酵赤灵芝总提取物注入猫的静脉之后,冠脉血流明显增加的同时,脑血流也增加。结扎豚鼠冠状动脉左旋支引起S-T段抬高,T波倒置的心电图改变,注射发酵赤灵芝总提取物,能使其恢复。这是降低了心肌耗氧量和可能增加了冠脉侧支血流进入缺血区的结果。用离体豚鼠心脏灌流实验,灵芝能扩张冠状动脉,对抗垂体后叶素引起的冠状血管收缩作用。灵芝能减低机体的耗氧量和明显提高小鼠耐低压缺氧的能力。用低压缺氧和离体心脏灌流实验表明,发酵生产的赤灵芝,野生赤灵芝和野生紫灵芝都有同样的药理作用,但用水提的效果不如酒提物和总生物硷有效。     

单胺氧化酶抑制剂苯乙肼对离体心脏的作用

用Langendorff离体心脏灌流法研究了苯乙阱对59只豚鼠和16只猫的冠脉流量、心搏率和心縮力的作用,并探討它与儿茶酚胺和5-羟基色胺(5-HT)的关系.(1)苯乙肼10^-6M对豚鼠搏动心脏有明显抑制,同时增加冠脉流量(+36%),其增加程度比在顫动心脏(+8%)更为明显,說明对搏动心脏增加冠脉流量的3/4是由于抑制心縮力而降低冠脉外阻力,另1/4是直接扩张冠脉的結果.对离体猫心的心搏率和心縮力无明显影响,因此在搏动和顫动心脏增加冠脉流量的程度近似(分別为+8%和+9%).(2)苯乙肼10^-6M灌流正常豚鼠心脏不但能消除脑垂体后叶素(0.5单位/升)減少冠脉流量(-23%)的作用,且使冠脉流量增加(+18%).預先腹腔注射苯乙肼(15毫克/公斤/天)連續6天的“苯乙肼化”豚鼠心脏使脑垂体后叶素收縮冠脉的反应基本消失.(3)苯乙肼对“利血平化”(經酪胺証实心脏內儿茶酚胺已被耗竭)的豚鼠和猫心的作用与对正常心脏的作用无明显差別,提示它的作用与释放儿茶酚胺关系較小.(4)“利血平化”的豚鼠心脏对5-HT的反应比正常者敏感.“苯乙肼化”和苯乙阱一次灌流后的豚鼠心脏对5-HT的反应均无显著加强,表明苯乙肼大概不是通过增加5-HT而扩张冠脉的.     

Cardiac action of KB-944, a new calcium antagonist

A comparative study was made between the cardiac action of diethyl 4-(benzothiazol-2-yl)benzylphosphonate (KB-944) and those of nifedipine, diltiazem and verapamil in anesthetized dogs and isolated right atria of guinea pigs. In anesthetized dogs, KB-944 caused a dose-dependent fall in mean blood pressure and dose-dependent increase in coronary sinus outflow. Coronary sinus outflow oxygen pressure was increased with increasing coronary sinus outflow; and consequently, the coronary arterio-venous oxygen difference was decreased. The cardiac output was slightly increased, while the myocardial oxygen consumption and myocardial work were reduced. In the isolated right atria of guinea pigs, KB-944 produced a decrease in spontaneous atria rate, and at the concentration of 10(-6) g/ml atrial standstill was seen in few preparations. The contractile force was decreased by KB-944. Especially, KB-944 exerted the weakest effect on contractile force among the tested drugs. These actions of KB-944 are very similar to those of nifedipine, diltiazem and verapamil.     

β2-Mediated Changes in Central Haemodynamics,Coronary Circulation and Myocardial Metabolism in Canine

Abstract: The combined effect of terbutaline on systemic and coronary circulation was investigated in dogs to clarify its influence on myocardial oxygen supply and lactate balance. The dogs were anaesthetized and the chest opened. Coronary sinus blood flow and cardiac output were monitored by thermodilution, aortic pressure was measured by tip-transducer and heart rate by RR-interval on ECG, coronary sinus blood were analyzed for lactate, oxygen and carbon dioxide. Terbutaline caused a substantial systemic vasodilation and an increased heart rate, the total external cardiac work increased to a minor degree. Terbutaline increased arterial lactate concentration. Coronary vascular resistance was reduced after terbutaline. Even if myocardial perfusion pressure was reduced and an increased external cardiac work was present, no signs of myocardial distress was observed in lactate metabolism or coronary sinus oxygen content. In fact a tendency to increased myocardial aerobic metabolism was observed, as myocardial lactate consumption increased after terbutaline. Terbutaline seems to be a coronary vasodilator in dogs. However, the demand for oxygen secondary to both an increase in cardiac work and aerobic metabolism can be harzardous to the potentially ischaemic myocardium.     

Effects of amiodarone with and without polysorbate 80 on myocardial oxygen consumption and coronary blood flow during treadmill exercise in the dog.

Since amiodarone has been reported to possess antianginal activity, this study examined the effects of amiodarone on coronary blood flow and myocardial oxygen consumption during exercise. Studies were performed in 14 chronically instrumented dogs trained to run on a motor-driven treadmill. Left circumflex coronary artery blood flow was measured with an electromagnetic flowmeter while aortic and coronary sinus catheters allowed measurement of myocardial oxygen extraction. During control conditions, graded exercise resulted in progressive increases in heart rate, aortic pressure, and coronary blood flow. Two preparations of amiodarone, 5 mg/kg, one dissolved in sterile water and the other in 10% polysorbate 80, were given intravenously to separate groups of dogs. Amiodarone in sterile water caused no hemodynamic changes at rest. However, the increase in heart rate during exercise was blunted after amiodarone, so that heart rate during the heaviest level of exercise was significantly less than during control exercise. Coronary blood flow and myocardial oxygen consumption were unchanged. Amiodarone with polysorbate 80 also blunted the increase in heart rate during exercise, but in addition caused a significant decrease in aortic pressure both at rest and during exercise. Myocardial oxygen consumption and coronary blood flow were significantly decreased after administration of amiodarone with polysorbate 80 at rest and during all exercise levels. Amiodarone with or without polysorbate 80 did not change myocardial oxygen extraction. These data demonstrate that amiodarone exerts a negative chronotropic effect during exercise. However, the decreased arterial pressure and myocardial oxygen consumption were not due to amiodarone, but was seen only with the combination of amiodarone dissolved in polysorbate 80.     

Cardiovascular actions of the dihydropyridine calcium antagonist nimodipine in the dog

When injected i.v. into anaesthetized, open-chest dogs, isopropyl (2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3, 5-pyridinedicarboxylate (nimodipine, Bay e 9736) (0.3-10 micrograms/kg) produced an increase in coronary sinus outflow and decreases in mean arterial blood pressure, coronary resistance, arterio-venous oxygen difference and heart rate in a dose-dependent manner, but virtually no change in myocardial oxygen consumption. At 3 micrograms/kg i.v. of the drug coronary resistance fell nearly to half the pre-drug value, coronary sinus outflow nearly doubled and heart rate decreased by about 10 beats/min. Myocardial oxygen consumption was slightly reduced at 30 micrograms/kg i.v. and atrioventricular (AV) conduction time was slightly increased at 10 and 30 micrograms/kg i.v. of the drugs. When the coronary vascular and cardiac effects of nimodipine were assessed in isolated, blood-perfused dog heart preparations, i.e., sinoatrial node, AV node and papillary muscle preparations, by intra-arterial administration, the following was revealed. In nearly twice the dose doubling coronary arterial blood flow, nimodipine produced a 15% decrease in sinus rate and a 15% increase in AV conduction time. However, in reducing the force of contraction of the papillary muscle by half the pre-drug value was needed nearly 17 times the dose of nimodipine doubling coronary arterial blood flow. Suppression of AV conduction by large doses of nimodipine was evident only when it was injected into the artery supplying the AV node but not into the artery supplying the His-Purkinje-ventricular system.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ouabain-induced ventricular tachycardia and its effect on the performance and metabolism of the dog heart

At constant pressure work there was an increase in the oxygen consumption of the dog heartlung preparation after tachycardia due to auricular stimulation and a far greater increase in consumption after ouabain-induced ventricular tachycardia, as compared with control hearts beating at their own sinus rhythm. In neither condition was the increase in coronary flow greater than the spontaneous increase in the controls. It is suggested that an increase in oxygen demand, under certain circumstances, may be met primarily by an increased desaturation of coronary blood. “Therapeutic” doses of ouabain did not improve the mechanical efficiency of the preparation. “Toxic” doses of ouabain which gave rise to ventricular tachycardia did not decrease the phosphocreatine or labile nucleotide phosphorus content of the heart provided there was no hypoxia of the heart muscle.     

Beta 2-mediated changes in central haemodynamics, coronary circulation and myocardial metabolism in canine

The combined effect of terbutaline on systemic and coronary circulation was investigated in dogs to clarify its influence on myocardial oxygen supply and lactate balance. The dogs were anaesthetized and the chest opened. Coronary sinus blood flow and cardiac output were monitored by thermodilution, aortic pressure was measured by tip-transducer and heart rate by RR-interval on ECG, coronary sinus blood were analyzed for lactate, oxygen and carbon dioxide. Terbutaline caused a substantial systemic vasodilation and an increased heart rate, the total external cardiac work increased to a minor degree. Terbutaline increased arterial lactate concentration. Coronary vascular resistance was reduced after terbutaline. Even if myocardial perfusion pressure was reduced and an increased external cardiac work was present, no signs of myocardial distress was observed in lactate metabolism or coronary sinus oxygen content. In fact a tendency to increased myocardial aerobic metabolism was observed, as myocardial lactate consumption increased after terbutaline. Terbutaline seems to be a coronary vasodilator in dogs. However, the demand for oxygen secondary to both an increase in cardiac work and aerobic metabolism can be hazardous to the potentially ischaemic myocardium.     

Coronary blood flow during exercise following nonselective and selective alpha 1-adrenergic blockade with indoramin

Studies were performed to compare the effects of alpha 1-adrenergic blockade with indoramin and nonselective alpha-adrenergic blockade with phentolamine on coronary blood flow and myocardial oxygen consumption during exercise. Nine dogs trained to run on a motor-driven treadmill were instrumented with electromagnetic flowmeter probes on the left circumflex coronary artery, and aortic and coronary sinus catheters for determination of myocardial arteriovenous oxygen difference. During control conditions, myocardial oxygen consumption and coronary blood flow increased as a direct function of heart rate during exercise. Phentolamine caused a significant decrease in blood pressure, while heart rate, coronary blood flow, and myocardial oxygen consumption were significantly increased at rest and during all exercise stages. Although alpha 1-adrenergic blockade with indoramin caused a similar reduction of arterial pressure, heart rate was unaltered both at rest and during exercise. Coronary blood flow and myocardial oxygen consumption were unchanged by alpha 1-adrenergic blockade at rest and during light exercise: however, during the heaviest exercise stages alpha 1-blockade caused a significant decrease in myocardial oxygen consumption. These findings are in agreement with the concept that phentolamine, by blocking presynaptic alpha 2-adrenoceptors which normally modulate norepinephrine release, increases sympathetic activity during exercise while indoramin, by acting as a selective alpha 1-adrenergic blocker, does not produce this effect.