3＇-大豆苷元磺酸钠对豚鼠离体右心房自律性及收缩特性的影响

目的研究3＇-大豆苷元磺酸钠对豚鼠离体右心房自律性及收缩特性的影响,并探讨其作用机制。方法采用豚鼠离体右心房测定3＇-大豆苷元磺酸钠对其自律性、收缩幅度、收缩速度、舒张速度的影响。结果3＇-大豆苷元磺酸钠可降低豚鼠离体右心房的自律性,明显降低豚鼠离体右心房的收缩幅度、收缩速度、舒张速度,且具有明显的剂量依赖性。结论3＇-大豆苷元磺酸钠可抑制豚鼠离体右心房的自律性,明显降低豚鼠离体右心房的收缩幅度、收缩速度、舒张速度,且具有明显的剂量依赖性。其作用机制可能与阻断电压依赖性Ca2＋通道及抑制肌浆网对Ca2＋的释放有关。     

拳参正丁醇提取物对豚鼠离体右心房自律性及收缩特性的影响

目的:研究拳参正丁醇提取物对豚鼠离体右心房自律性及收缩特性的影响。方法:采用豚鼠离体右心房测定拳参正丁醇提取物对其自律性、收缩幅度、收缩速度、舒张速度的影响。结果:拳参正丁醇提取物可降低豚鼠离体右心房的自律性,明显降低豚鼠离体右心房的收缩幅度、收缩速度、舒张速度,且具有明显的剂量依赖性。结论:拳参正丁醇提取物可抑制豚鼠离体右心房的自律性,明显降低豚鼠离体右心房的收缩幅度、收缩速度、舒张速度。     

拳参正丁醇提取物对豚鼠心肌生理特性的影响

目的研究拳参正丁醇提取物对豚鼠离体右心房自律性及收缩特性的影响，并探讨其作用机制。方法采用豚鼠离体右心房测定拳参正丁醇提取物对其自律性、收缩幅度、收缩速度、舒张速度的影响。结果拳参正丁醇提取物可降低豚鼠离体右心房的自律性，降低豚鼠离体右心房的收缩幅度、收缩速度、舒张速度，且具有明显的剂量依赖性。结论拳参正丁醇提取物可抑制豚鼠离体右心房的自律性，降低豚鼠离体右心房的收缩幅度、收缩速度、舒张速度，且具有明显的剂量依赖性。其机制可能与抑制钙离子的内流及改变肌浆网上的钙泵活性有关。     

灯盏花素对豚鼠离体右心房自律性及收缩特性的影响

目的:观察灯盏花素对豚鼠离体右心房自律性及收缩特性的影响。方法:采用豚鼠离体右心房测定灯盏花素对其自律性、收缩幅度、收缩速度、舒张速度的影响。结果:灯盏花素对豚鼠离体右心房的自律性无明显影响,但可降低心房肌的收缩幅度、收缩速度、舒张速度,且有明显的剂量依赖性。结论:灯盏花素可明显降低豚鼠离体右心房的收缩幅度、收缩速度、舒张速度。     

3''''-大豆苷元磺酸钠对豚鼠胆囊收缩运动的影响

目的:研究3'-大豆苷元磺酸钠对胆囊收缩运动的影响。方法:通过对豚鼠胆囊肌条观察3'-大豆苷元磺酸钠拮抗组胺所致胆囊收缩运动、拮抗高K 所致胆囊收缩运动、拮抗Ca2 引起豚鼠离体胆囊收缩运动、拮抗乙酰胆碱所致胆囊收缩运动的影响。结果:3'-大豆苷元磺酸钠可明显拮抗组胺、高K 所致胆囊收缩运动及拮抗累积Ca2 引起豚鼠离体胆囊收缩运动,但对乙酰胆碱所致胆囊收缩运动无影响。结论:3'-大豆苷元磺酸钠可明显拮抗组胺、高K 、Ca2 引起豚鼠离体胆囊收缩。     

3＇-大豆苷元磺酸钠对豚鼠胆囊收缩运动的影响

目的：研究3＇-大豆苷元磺酸钠对胆囊收缩运动的影响。方法：通过对豚鼠胆囊肌条观察3＇-大豆苷元磺酸钠拮抗组胺所致胆囊收缩运动、拮抗高K^＋所致胆囊收缩运动、拮抗Ca^＋引起豚鼠离体胆囊收缩运动、拮抗乙酰胆碱所致胆囊收缩运动的影响。结果：3＇-大豆苷元磺酸钠可明显拮抗组胺、高K^＋所致胆囊收缩运动及拮抗累积Ca^＋引起豚鼠离体胆囊收缩运动，但对乙酰胆碱所致胆囊收缩运动无影响。结论：3＇-大豆苷元磺酸钠可明显拮抗组胺、高K^＋、Ca^＋引起豚鼠离体胆囊收缩。     

大豆苷元对豚鼠胆囊收缩运动及机制的研究

目的:研究大豆苷元对胆囊收缩运动的影响及其机制.方法:以豚鼠离体胆囊肌条收缩强度为指标,观察不同浓度的大豆苷元对豚鼠离体胆囊肌条自发性收缩及其对乙酰胆碱、组织胺、高K 和高Ca2 所致胆囊收缩运动的影响.结果:大豆苷元能显著抑制豚鼠离体胆囊肌条的自发性收缩活动,使收缩力降低,紧张性下降,且呈量效反应关系.大豆苷元还可明显拮抗乙酰胆碱、组胺、高K 所致胆囊收缩运动及拮抗累积Ca2 引起豚鼠离体胆囊收缩运动.结论:大豆苷元能显著抑制豚鼠离体胆囊自发性收缩,此作用可能与拮抗胆碱能受体、组胺受体、高K 、Ca2 或对豚鼠离体胆囊平滑肌的直接作用有关.     

大豆苷元对豚鼠胆囊收缩运动的影响

目的:研究大豆苷元对胆囊收缩运动的影响.方法:采用豚鼠胆囊肌条观察大豆苷元拮抗乙酰胆碱、组胺、高K 、Ca2 所致豚鼠离体胆囊收缩运动的影响.结果:大豆苷元可明显拮抗乙酰胆碱、组胺、高K 所致胆囊收缩运动及拮抗累积Ca2 引起豚鼠离体胆囊收缩运动.结论:大豆苷元可明显拮抗豚鼠离体胆囊收缩.     

3'-大豆苷元磺酸钠对离体心脏缺血再灌注损伤的保护作用

目的利用离体心脏灌流模型,研究3'-大豆苷元磺酸钠对离体心脏缺血再灌注后损伤的保护作用。方法应用大鼠离体心肌缺血再灌注损伤模型,在灌流液中加入高、低剂量的3'-大豆苷元磺酸钠(0.03,0.01mg/L)。测定冠脉流量、心率、左心室收缩压、左心室舒张压的变化。结果3'-大豆苷元磺酸钠可使缺血再灌注后心脏灌流量增大、左心室收缩压增大、左心室舒张压降低、心率减慢。结论3'-大豆苷元磺酸钠可通过扩张冠脉、减慢心率及增强心肌收缩力对离体心脏缺血再灌注损伤起保护作用。     

3’-大豆苷元磺酸钠对大鼠脑缺血再灌注肾脏损伤保护作用的研究

目的 观察3'-大豆苷元磺酸钠对大鼠脑缺血再灌注肾脏损伤保护作用的研究.方法取雄性Wistar大鼠32只,随机分为4组,每组8只,分别为假手术组,缺血再灌注组,3'-大豆苷元磺酸钠低、高剂量组.观察大鼠脑缺血再灌注后肾脏病理组织变化及有关指标改变.结果 3'-大豆苷元磺酸钠对脑缺血再灌注损伤大鼠肾脏有明显保护作用,且呈一定的剂量依赖性.结论 3'-大豆苷元磺酸钠对大鼠心肌缺血再灌注肾脏损伤具有一定的保护作用.     

槐花对家兔体外心房肌的作用

目的 :观察槐花对家兔体外心房肌生理特性的影响 ,并探讨其作用机制。方法 :运用体外心脏实验法 ,摘取家兔心房肌 ,观察测定给药前后体外心房肌的收缩力、心率、功能性不应期、静息后加强及正性阶梯效应的变化。结果 :槐花煎液能显著降低心肌收缩力、减慢心率 ,阿托品可抑制槐花的负性心率作用 ,但不能抑制其负性肌力作用 ;槐花煎液可显著减弱家兔体外左心房肌的正性阶梯作用 ,并显著延长功能性不应期 ,但不影响静息后加强效应。结论 :槐花对心肌具有负性肌力和负性频率作用 ,其作用机制与其抑制胞外 Ca2 +跨膜内流有关。     

侧柏叶乙酸乙酯提取物对豚鼠离体气管平滑肌的作用

用离体豚鼠气管条,探讨侧柏叶乙酸乙酯提取物对气管平滑肌作用。结果表明,侧柏叶乙酸乙酯提取物能抑制乙酰胆碱,氯化钾所致气管平滑肌收缩,而且能使乙酰胆碱收缩气管平没肌的量效曲线右移,并抑制最大效应,其作用为剂量依赖性心肌肥厚提示侧柏叶乙酸乙酯提取物松驰气管平滑肌作用机制可能与影响Ｃａ＾２＋的跨膜转运有关。     

Scutellarin-induced endothelium-independent relaxation in rat aorta

Scutellarin is a flavonoid extracted from the traditional Chinese herb, Erigeron breviscapus Hand Mazz. In the present study, the vasorelaxant effects of scutellarin and the underlying mechanism were investigated in isolated rat aorta. Scutellarin (3, 10, 30, 100 microm) caused a dose-dependent relaxation in both endothelium-intact and endothelium-denuded rat aortic rings precontracted with noradrenaline bitartrate (IC(50) = 7.7 +/- 0.6 microm), but not with potassium chloride. Tetraethylammonium, glibenclamide, atropine, propranolol, indomethacin and N(G)-nitro-l-arginine methyl ester had no influence on the vasorelaxant effect of scutellarin, which further excluded the involvement of potassium channels, muscarinic receptor, nitric oxide pathway and prostaglandin in this effect. Pretreatment with scutellarin decreased the tonic phase, but not the phasic phase of the noradrenaline bitartrate induced tension increment. Scutellarin also alleviated Ca(2+)-induced vasoconstriction in Ca(2+)-depleted/noradrenaline bitartrate pretreated rings in the presence of voltage-dependent calcium channel blocker verapamil. The noradrenaline bitartrate evoked intracellular calcium increase was inhibited by scutellarin. Scutellarin had no effect on phorbol-12,13-diacetate induced contraction in a calcium-free bath solution. These results showed that scutellarin could relax thoracic artery rings in an endothelium-independent manner. The mechanism seems to be the inhibition of extracellular calcium influx independent of the voltage-dependent calcium channel.     

Investigations to characterize the antiarrhythmic action of bergamottine,a furocoumarin isolated from bergamot oil

Bergamottine is a furocoumarin isolated from the non-volatile essential oil of Citrus bergamia Risso (Bergamot, Rutaceae) with antiarrhythmic properties. We investigated and classified its mechanism of action according to Vaughan Williams. We have found that bergamottine at a concentration range of 5–20 μg/mL (14.7–59 μM ) decreased the frequency and the force of the contraction in spontaneously beating guinea-pig right atria and electrically paced left atria in a concentration-dependent manner. Furthermore this furocoumarin caused a parallel shift of the dose-response curve to CaCl₂ similar to that of verapamil in the electrically driven left atrium, indicating a possible Ca-antagonistic property. Bergamottine (1 mg/kg i.v.) significantly prolonged the atrioventricular conduction time, the corrected sinus-node recovery time and the corrected sinus-atrial conduction time in anaesthetized rabbits. Bergamottine did not inhibit isoprenaline-induced positive chronotropic responses in atrial muscle, indicating that it has no β-blocking activity, and did not show significant local-anaesthetic property in the guinea-pig intradermal wheal test. These results demonstrate that bergamottine seems to be an antiarrhythmic drug having class IV (inhibitor of calcium transport) type activity. © 1997 John Wiley & Sons, Ltd.     

Effect of an aqueous extract of Portulaca oleracea leaves on smooth muscle and rat blood pressure

An aqueous extract of Portulaca oleracea leaves and stems produced a dose-dependent relaxation of guinea pig fundus, taenia coli and rabbit jejunum and a dose-dependent contraction of the rabbit aorta. On spontaneously-beating rabbit right atria and electrically-paced left atria, the extract produced a dose-dependent negative inotropic and chronotropic effects. On rat blood pressure, the extract produced dose-dependent pressor responses. Phentolamine reduced the relaxant effect of the extract on gut smooth muscle and abolished the contractile response on the aorta as well as the pressor response on blood pressure. Guanethidine and tetrodotoxin had no effect on extract-induced relaxant or contractile responses. On rat blood pressure atropine and cyproheptadine had no effect on extract-induced pressor response, whereas propranolol slightly reduced the pressor response. An increase in extracellular calcium reversed the inhibitory effect of the extract on the rabbit atria. The extract may, therefore, act in part on postsynaptic alpha-adrenoceptors and by interference with transmembrane calcium influx.     

Analysis of the mechanisms underlying the vasorelaxant action of coptisine in rat aortic rings

The aim of the present study was to evaluate the vasorelaxant effects of coptisine and its possible mechanisms in isolated rat aortic rings. Coptisine was evaluated on isolated rat aortic rings precontracted with norepinephrine (NE) and KCl. The mechanisms were evaluated in the presence or absence of specific pharmacological inhibitors. Coptisine (1 ~ 200 μM) relaxed NE (1 μM) or KCl (60 mM) induced sustained contraction with pEC(50) values of 4.49 ± 0.48 and 4.85 ± 0.57 in a concentration dependent manner. Pretreatment with coptisine (10, 50 or 100 μM) also inhibited concentration-response curves to NE and KCl. The vasorelaxant effect of coptisine was attenuated significantly by endothelium removal, and incubation with Nω-nitro-L-arginine methyl ester (L-NAME, 100 μM), methylene blue (10 μM) and indomethacin (5 μM) partially reduced the vasorelaxant effect of coptisine. In endothelium-denuded rings, the vasorelaxant effect of coptisine was reduced significantly by 4-aminopyridine (4-AP, 100 μM), but not glibenclamide (10 μM) ortetraethylammonium (TEA, 5 mM). Coptisine also reduced NE-induced transient contraction in Ca(2+)-free solution, and inhibited contraction induced by increasing external calcium in Ca(2+)-free medium plus 60 mM KCl. It was concluded that coptisine induced both endothelium-dependent and -independent relaxation in rat aortic rings. The NO-cGMP mediated pathway may be involved in the endothelium-dependent relaxation and in the activation of voltage-dependent K(+) channels, contributing in part to the endothelium-independent relaxation bycoptisine. Coptisine also blocks extracellular Ca(2+) influx by interacting with both voltage- and receptor-operated Ca(2+) channels.     

The cardiovascular depression caused by bee venom in Sprague-Dawley rats associated with a decrease of developed pressure in the left ventricular and the ratio of ionized calcium/ionized magnesium

Bee venom (BV) has been used in Oriental medicine to treat inflammatory diseases, such as tendonitis, bursitis, and rheumatoid arthritis, despite the sensitivity of the victims and toxicity of the venom. This study examined the mechanisms for the effects of BV on the cardiovascular system in rats. The arterial pressure and heart rate (HR) were measured in anesthetized rats. In addition, the left ventricular development pressure (LVDP) and total magnesium efflux ([Mg]e) in isolated perfused hearts, the vascular tonic responses in the isolated aorta, and the blood ionic and biochemical changes were determined simultaneously. In the anesthetized rats, the mean arterial pressure, systolic pressure, and pulse pressure were reduced by BV in a dose-dependent manner, even though the HR was increased. BV had no effects on the relaxation of phenylephrine- or KCl-induced contraction of the aortic rings. In the isolated hearts, BV generated a reversible decrease in the LVDP and velocity with changes in pressure, which were accompanied by increases in the HR and [Mg]e. BV increased the plasma ionized and total magnesium concentrations, and decreased the total magnesium level in the red blood cells. The ratio of ionized calcium/ionized magnesium was also decreased by the BV treatment. BV caused a detectable increase in blood creatine kinase, glutamic oxaloacetic transaminase, and lactic dehydrogenase, as well as a decrease in the blood total protein albumin and globulin levels. These results suggest that BV induces cardiovascular depression by decreasing the cardiac pressure and increasing the ionized magnesium concentration in the blood.     

Anti-diarrheal and spasmolytic activities and acute toxicity study of Soonkijangquebo, a herbal anti-diarrheal formula

The anti-diarrheal and spasmolytic activities of Soonkijangquebo (SKJQB), a Korean herbal anti-diarrheal formulation, were subjected to pharmacological evaluation. SKJQB, at a dose of 50-200 mg/kg, inhibited castor oil-induced diarrhea in mice. The median effective dose (ED50) for the anti-diarrheal effect was 93 mg/kg. In isolated rabbit jejunum preparations, SKJQB produced a spasmolytic effect by the relaxation of spontaneous contractions in a dose-dependent manner. The median effective concentration (EC50) for the spasmolytic effect was 3.6 mg/ml. In isolated guinea pig ileum preparations, SKJQB also produced a spasmolytic effect by reduction of acetylcholine-induced contractions. When tested against calcium channel blockade in rabbit jejunum, SKJQB caused a dose-dependent rightward shift in the Ca2+ dose-response curves, similar to that produced by verapamil, a well-known calcium antagonist. In an acute toxicity study in Sprague-Dawley rats, the median lethal dose (LD50) of SKJQB was greater than 2000 mg/kg, and no pathological changes were noticed in macroscopic examination by necropsy of rats treated with SKJQB. Thus, SKJQB may be safely used as a spasmolytic as well as an anti-diarrheal agent.     

环维黄杨星D与哇巴因等药合用对离体心肌收缩力的影响

 环维黄杨星D(CVB-D)1～10μmol/L和哇巴因合用后,离体豚鼠心肌收缩力增强,收缩和舒张时间缩短,平均收缩速度和舒张速度加快,最大反应增加? CVB-D1～10umol/L增强异丙肾上腺素?去氧肾上腺素?组胺和 CaCl₂的正性肌力作用,使其量效曲线左移,最大反应增加? CVB-D能对抗维拉帕米和 Ach5umol/L所致的负性肌力作用?结果表明,CVB-D正性肌力作用的机理可能与 a?β和 H₂-受体?电压依赖钙通道激动剂及哇巴因不同,而与促进心肌细胞外Ca²⁺内流和抑制内K+外流有关?