蜂毒素对大鼠离体心房的作用

目的：研究蜂毒素（Ｍｅｌ）对大鼠心脏的作用．方法：采用大鼠离体心房，测定给药前后心房率，心收缩力，左房休息后加强及阶梯现象．结果：Ｍｅｌ２００ｍｇ·Ｌ－１对大鼠右心房产生正性频率作用，可被Ｖｅｒ０１μｍｏｌ·Ｌ－１拮抗．Ｍｅｌ２５ｍｇ·Ｌ－１抑制左心房休息后加强，并使正性阶梯现象产生翻转．Ｍｅｌ抑制左右心房收缩力．结论：Ｍｅｌ具正性频率作用和负性肌力作用．     

血管紧张素转化酶抑制剂卡托普利对健康心脏工作的影响

血管紧张素转化酶抑制剂（ＡＣＥＩ）因其能够减弱血管抗性,降低血压,而广泛用于高血压病人,但很少考虑其对心脏的损伤作用。ＡＣＥＩ影响不同组织局部肾素－血管紧张素系统,其作用的两种主要机理是：（１）抑制血管紧张素Ⅱ的合成。血管紧张素Ⅱ是一种可增加收缩力和改变收缩时象的肽类激素。长期应用,血管紧张素可作为心肌生长因子。抑制血管紧张素Ⅱ合成时出现血管紧张素片段的积聚,产生扩张冠状动脉的作用。（２）减少缓激肽（ｂｒａｄｙｋｉｎｉｎ,ＢＫ）的降解。ＢＫ在缺血性心脏和肥大心脏中可增加冠脉血流,增强收缩力,减少…     

药理学

053.用由血液灌注的离体狗心乳头肌同时测定冠状血管扩张药物对冠状血流和心脏收缩力的影响据认为,冠状血管扩张药的负性收缩能作用有利于缺血性心脏病的治疗。因为降低心肌收缩力可降低氧耗量。然而,负性收缩能作用过强可导致充血性心力衰竭。所以,对     

美托洛尔对高血压性心脏病患者不同时间段的QT间期离散度及室性心律失常发生率影响研究

<正>高血压性心脏病是由于血压长期升高导致心脏后负荷过重所诱发的心脏损害。目前在临床上治疗高血压性心脏病最有效的药物是美托洛尔,它对β_1-受体有阻断作用,可以降低血压、减慢心率、抑制心收缩力、降低自律性等,从而减少室性心律失常的发生率,降低病死率~([1])。在本研究中,观察美托洛尔对283例高血压性心脏病患者,在不同时段的QT间期离散度(QTd)及室性心律失常发生率的影响变化情况,分析如下。     

β受体阻滞剂及其治疗高血压现状探讨

β受体阻滞剂是临床治疗高血压的常用药物,在控制血压的同时还具有降低心肌收缩力、心肌需氧量、心输出量以及抑制外周肾上腺能受体等作用。β受体阻滞剂被认为是目前临床治疗高血压的一线治疗药物。近年来,β受体阻滞剂对于高血压的影响研究获得了较大进展,但关于其治疗地位以及作用机制仍存在一定的争议。本文就β受体阻滞剂的作用机理、应用优势以及临床应用研究进展进行综述。     

如何安全合理使用维拉帕米

维拉帕米又称异搏定,是一种非二氢吡啶类钙离子拮抗剂。该药能够有选择性地阻滞心肌和血管平滑肌细胞膜上的钙离子通道,抑制窦房结和房室结的功能,从而起到减弱心肌收缩力、扩张血管、降低血压、降低窦房结的自律性及减慢心率的作用。     

氨茶碱临床使用案例分析

氨茶碱为茶碱与乙二胺复合物,其药理作用主要来自茶碱,乙二胺可增加茶碱的水溶性.主要作用有松弛支气管平滑肌,抑制过敏介质释放;增强呼吸肌的收缩力,减少呼吸肌疲劳;增强心肌收缩力,增加心输出量,低剂量一般不加快心率;舒张冠状动脉、外周血管和胆管;增加肾血流量,提高肾小球滤过率,减少肾小球对钠和水的重吸收,具有利尿作用[1].在日常使用中,总结一些使用案例,提高对氨茶碱的正确应用.     

钩藤碱对离体豚鼠心脏电活动的影响

钩藤碱(Rhynchophylline,Rhy)具有降低血压、扩张血管、减慢心率和抑制心肌收缩力等作用;实验表明其松弛血管和子宫平滑肌的作用与钙拮抗有关.为了进一步探讨其对心脏的负性频率及负性肌力作用机制,本文报道Rhy对离体豚鼠灌流心脏电活动影响的初步观察.     

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.     

藜芦属植物化学成分的研究近况

综述我国藜芦属植物在化学成分和药理及临床方面的研究进展。藜芦属植物主要含甾体生物碱、芪类化合物等。药理研究证实其甾体生物碱具有增强心肌收缩力、降低血压、抗血栓等作用；芪类化合物具有：抗肿瘤、抑制血小板凝结作用。中医早已将某些藜芦属植物入药。     

Cardiovascular actions of mixidine fumarate

Mixidine has been reported to slow the heart rate without decreasing the force of myocardial contraction. In view of force-frequency relationships, it may have a ‘masked’ positive inotropic action which counter-balances the decrease in the force of contraction secondary to its cardiac slowing effect. Thus, the effect of this compound on the mammalian cardiovascular system was examined in several heart preparations. Mixidine reduced heart rate in anesthetized cats with a transient increase in blood pressure. In spontaneously beating Langendorff preparations of guinea-pig heart and in canine heart-lung preparations, it caused a sustained decrease in the heart rate with a concomitant decrease in force of contraction. In right atrial preparations of guinea-pig heart, however, the mixidine-induced fall in heart rate was not accompanied by changes in force of contraction. In electrically stimulated left atrial preparations of guinea-pig heart and canine heart-lung preparations, mixidine produced a positive inotropic effect. The inotropic effect observed in guinea-pig atrial preparations was not influenced by a concentration of propranolol which could significantly shift the concentration-response curve for isoproterenol. The positive inotropic effect of mixidine observed in canine heart-lung preparations was greater when it was given into left atrium, bypassing pulmonary circulation, or in preparations depressed with pentobarbital. These results indicate that mixidine has a positive inotropic effect in addition to its cardiac slowing action. Thus, the net effect of this drug on force of myocardial contraction depends on the relative contributions of the direct positive inotropic effect and an indirect negative inotropic effect secondary to cardiac slowing. A compound which has these properties may be useful in treating ischemic heart disease.     

王不留行总黄酮对离体蛙心心肌收缩力和心率的影响

目的: 探讨王不留行总黄酮对离体蛙心的影响及可能的作用机制。方法: 采用斯氏蛙心灌流法制备离体蛙心标本,待离体蛙心收缩力稳定后,分别加入不同浓度的王不留行总黄酮、阿托品、盐酸异丙肾上腺素,观察这些药物对离体蛙心收缩活动的影响。结果: 总黄酮在0.02~0.10 mg·mL^-1范围内,随着王不留行总黄酮浓度的增大,离体蛙心心肌平均收缩力与给药前相比较明显减小(P<0.05或P<0.01);心率与给药前相比较,仅0.08 mg·mL^-1和0.10 mg·mL^-1剂量组与给药前比较减慢差异明显(P<0.05或P<0.01);心肌最大收缩力与给药前相比较,除0.04 mg·mL^-1剂量组外,其他4组与给药前比较均有明显抑制作用(P<0.01)。随着细胞外钙离子浓度的逐渐增大,王不留行总黄酮对蛙心心肌平均收缩力的抑制率逐渐增大(P<0.05或P<0.01),加入阿托品和盐酸异丙肾上腺素后提取液对离体蛙心的抑制作用有所降低。结论: 王不留行总黄酮对离体蛙心活动有一定的抑制作用,作用机制可能与钙离子通道有关,与心肌细胞膜上受体关系有待进一步研究。     

Are the prejunctional histamine receptors on sympathetic nerve terminals in guinea-pig isolated atria activated during anaphylaxis in vitro?

In isolated atria from sensitized guinea-pigs, antigenic challenge with ovalbumin induces an anaphylactic reaction in which there is an increased rate and force of contraction. At the same time, stimulation-induced release of [3H] noradrenaline is inhibited by 40%. Cimetidine decreased the tachycardia occurring during anaphylaxis but no effect on the inhibition of stimulation-induced transmitter release. It is known that antigenic challenge of sensitized guinea-pig atria release histamine from mast cells; this histamine acts postjunctionally to increase heart rate. However, the inhibition of noradrenergic transmitter release is not due to the stimulation of prejunctional inhibitory histamine receptors.     

Muscarinic receptors in the failing human heart.

In the human heart, as in the heart of several other species, muscarinic receptors are predominantly of the M2-subtype that couple via a pertussis toxin-sensitive Gi-protein to inhibit adenylyl cyclase. However, it is not clear whether an additional muscarinic receptor subtype exists in the human heart. In human right atrium, stimulation of muscarinic M2 receptors causes direct negative inotropic and chronotropic effects; in human ventricular myocardium, however, the negative inotropic effect can be only achieved when basal force of contraction has been pre-stimulated by cyclic AMP-elevating agents such as beta-adrenoceptor agonists, forskolin or phosphodiesterase inhibitors (indirect effect); this has been shown in various in vitro and in vivo studies. Evidence has accumulated that in chronic heart failure vagal activity is decreased. Cardiac muscarinic M2 receptor density and functional responsiveness (inhibition of adenylyl cyclase activity and negative inotropic effects), however, are not considerably changed when compared with non-failing hearts although cardiac Gi-activity is increased.     

A comparison of the cardiovascular effects of diphenylthiohydantoin and diphenylhydantoin

The comparative effects of diphenylthiohydantoin and diphenylhydantoin on the cardiovascular system of the cat were revaluated in Dial-urethane-anesthetized preparations by monitoring (1) the right ventricular contractile force, (2) the femoral arterial pressure, and (3) the electrocardiogram. I.V. injections of each drug (2, 4, 8 and 16 mg/kg) caused dose dependent decreases in contractile force, blood pressure, and heart rate. However, cardiac depression produced by diphenylthiohydantoin was significantly less than the cardiac depression produced by diphenylhydantoin. With respect to reduction in blood pressure and heart rate, the two drugs were found to be equipotent. In addition, both drugs were equally effective in converting deslanoside-induced ventricular tachycardia to sinus rhythm. These results indicate that diphenylthiohydantoin has an advantage over diphenylhydantoin for the treatment of cardiac arrhythmias because it does not depress the pumping function of the heart as profoundly as diphenylhydantoin.     

多沙唑嗪以及阿夫唑嗪对映体对小鼠离体心房心率和收缩力的影响

目的分析多沙唑嗪以及阿夫唑嗪的光学异构体及其外消旋体与药物调节小鼠离体心房心率和心肌收缩力效应的关系。方法制备小鼠离体左心房和离体右心房标本,观察消旋多沙唑嗪[(±)DOX]、左旋多沙唑嗪[(-)DOX]、右旋多沙唑嗪[(+)DOX]、消旋阿夫唑嗪[(±)ALF]、左旋阿夫唑嗪[(-)ALF]以及右旋阿夫唑嗪[(+)ALF]对小鼠离体右心房心率及左心房心肌收缩力的影响。结果 (+)DOX组的16例标本中,加入30μmol·L-1药物后,5例(31.3%)发生停搏;(±)DOX组、(-)DOX组各有1例发生停搏;其他各组标本未出现停搏反应。(+)DOX和(±)DOX各浓度均减慢小鼠右心房心率(P<0.01),并具有浓度依赖关系;(+)DOX减慢心率的作用强于同浓度(±)DOX(P<0.01)。10和30μmol·L-1浓度的(-)DOX减慢心率(P<0.01),其作用弱于同浓度(+)DOX(P<0.01)。(-)ALF、(+)ALF及(±)ALF在10和30μmol·L-1浓度时均轻度减慢小鼠右心房心率(P<0.05)。在小鼠离体左心房标本,(+)DOX(10和30μmol·L-1)抑制心肌收缩力(P<0.05);而(-)DOX(3～30μmol·L-1)增强心肌收缩力(P<0.05),其增强作用强于同浓度(±)DOX(P<0.05)。(±)ALF及其对映体(3～30μmol·L-1)对小鼠离体左心房心肌收缩力无影响。结论 DOX对小鼠离体心房的心率和心肌收缩力具有明显的影响,高浓度尚可诱发心脏停博反应;DOX的手性结构对其上述活性具有明显的影响。相反,ALF仅影响小鼠心率,ALF的手性结构对其心脏效应无明显影响。     

Pharmacological analyses of hydralazine-induced cardiac action in intact dogs and isolated, blood-perfused canine atria

The effects of hydralazine (HYD) on heart rate and blood pressure in the intact dog and on atrial rate and contractile force in the isolated atrium were investigated. HYD (0.1-1 mg) injected into the sinus node artery produced double peaked positive inotropic and negative chronotropic effects in a dose-related manner. The initial positive inotropic and negative chronotropic responses were not affected by propranolol and atropine, respectively. The second positive inotropic response was inhibited by propranolol or reserpine, but it was not suppressed by imipramine or tetrodotoxin. When HYD (0.1-1 mg/kg) was administered intravenously to the donor dog, an initial increase followed by a decrease in blood pressure and an increase in heart rate were observed. In the isolated atrium, an increase in contractile force was induced. The increases of blood pressure and heart rate in the donor dog and the positive inotropic effect in the isolated atrium after HYD treatment were suppressed by reserpine. These results suggest that HYD has direct positive inotropic and negative chronotropic effects and indirect cardiac stimulating effects caused by a release of catecholamines from sympathetic nerve terminals, and that HYD-induced catecholamine release is not mediated by a tyramine-like action or via nerve excitation.     

The cardiovascular actions of WR-149,024 (1,18-diamino-7,13-diaza-9,10-dithiaoctadecane tetrahydrochloride)

1. The general cardiovascular properties of WR-149,024 (a straight chain sulphur-containing aliphatic amine) in dogs and cats are reported.2. Intravenous administration of this compound produced an immediate hypotension and bradycardia in intact anaesthetized dogs. These effects were independent of the parasympathetic nervous system since they were also present in atropinized and bilaterally vagotomized dogs.3. Ascending aortic blood flow increased after administration of WR-149,024 despite a reduction in blood pressure, contractile force and heart rate. It appears that the initial hypotension is due to a decrease in total peripheral vascular resistance since WR-149,024 produced relatively little change in force of contraction or heart rate in the isolated, blood-perfused heart preparation.4. WR-149,024 reversed the pressor effects of adrenaline within 10 min of injection while at the same time the vasopressor response to angiotensin or the vasodepressor response to isoprenaline was not altered. alpha-Adrenoceptor blockade was still evident up to five days after dosing.5. WR-149,024 did not block phenylephrine inhibition of intestinal motility. These findings suggest that WR-149,024 initiates a relatively specific and prolonged alpha-adrenoceptor blockade.     

Effect of Krebs cycle metabolites on frog heart.

All the Krebs metabolites except pyruvate, lactate, acetate and succinate reduced the force and rate of myocardial contractions and also decreased cardiac output in frog. Succinate on the contrary was found to augment the rate and force of heart. The cardiac stimulation produced by epinephrine was reduced by fumarate, malate, oxaloacetate and alpha-oxoglutarate, whereas transaconitate and citrate produced only a slight inhibition. Pyruvate, lactate, acetate and succinate did not alter cardiac response to epinephrine.     

A GABA cardiovascular mechanism in the dorsal raphe of the rat

An injection of gamma-aminobutyric acid (GABA) and the GABA agonist, muscimol, into the dorsal raphe reduced both heart rate and blood pressure in the urethane-anesthetized rat. Picrotoxinin (3.4 nmol) did not affect blood pressure and slightly reduced the heart rate when injected into the dorsal raphe, but it blocked the decrease in both cardiovascular responses produced by GABA. These decreases in heart rate and blood pressure most likely result from stimulation of a GABAA receptor, as the GABAB agonist, baclofen, appeared to elevate heart rate and blood pressure by a mechanism occurring outside the dorsal raphe area. The changes in blood pressure and heart rate induced by muscimol occurred whether or not respiration was supported. Finally, it can be inferred that these GABAergic actions on blood pressure and heart rate probably involve both an inhibition of central sympathetic outflow and an excitation of parasympathetic outflow, as the quaternary muscarinic blocker, atropine methyl nitrate, blocked the decrease in heart rate induced by muscimol, but not the decrease in blood pressure.