水飞蓟宾抗再灌注心律失常及清除超氧阴离子的作用

本实验观察到水飞蓟宾口服及静脉注射均可使大鼠再灌注心律失常明显减少。利用电子自旋共振测定发现水飞蓟宾的口服粉剂及静脉注射剂（水飞蓟宾葡甲胺盐）均可使体外产生的超氧阴离子明显减少。推测水飞蓟抗再灌注心律失常作用可能与其抗自由基作用有关。     

茵芩清肝汤对酒精诱导的大鼠急性肝损伤保护作用的探讨

[目的]探讨茵芩清肝汤对酒精诱导的急性肝损伤的保护作用.[方法]将100只实验大鼠随机按处理不同分为5组(每组20只):茵芩清肝汤组、硫普罗宁组、水飞蓟宾胶囊组、模型对照组和空白对照组;观察茵芩清肝汤对模型大鼠血生化、肝脏病理学各指标的影响,并与其他各组进行比较.[结果]经酒精诱导,模型对照组大鼠肝指数明显增加、转氨酶明显上升,血清一氧化氮明显升高,谷胱甘肽-过氧化物酶明显降低.茵芩清肝汤组、硫普罗宁组、水飞蓟宾胶囊组较模型对照组大鼠肝组织损伤轻,茵芩清肝汤组肝脏指数明显降低,与模型对照组和水飞蓟宾胶囊组比较有显著性差异;茵芩清肝汤组能明显降低一氧化氮、提高谷胱甘肽-过氧化物酶活性,与模型对照组、硫普罗宁组比较差异有统计学意义;病理切片显示,茵芩清肝汤组大鼠肝索及肝血窦结构清晰,肝细胞仅为轻度或中度水肿.[结论]茵芩清肝汤能降低肝脏氧化应激和脂质过氧化的影响,改善肝脏病理变化,提示对酒精诱导的大鼠急性肝损伤具有保护作用.     

水飞蓟宾在非酒精性脂肪性肝炎进展过程中对肝纤维化的影响

目的研究水飞蓟宾对NASH大鼠肝纤维化进展的影响。方法30只雄性SD大鼠随机分为正常饮食对照组（n=10）、高脂饮食模型组（n=10）和水飞蓟宾治疗组（n=10），实验时间12周。生化法检测血清AST，ALT，TG，CHO。放免法检测HA，RTPCR法检测TIMP-1、TIMP-2、MMP-2、MMP-13mRNA的表达，紫外分光光度计测量SOD及MDA。结果与模型组比较，水飞蓟宾治疗组大鼠肝功改善，HA及SOD含量下降，TIMP-1、TIMP-2、MMP-2表这降低，MMP-13及MDA升高，肝纤维化程度减轻。结论水飞蓟宾具有一定抗纤维化作用。     

溴苄胺治疗并发于急性心肌梗塞的复发性心室颤动

溴苄胺(Bretylium tosylate)属于肾上腺能阻滞剂,具有独特的抗心律失常作用。Bacaner等证明该药可提高实验动物狗的室颤阈;同时在临床上也能有效的控制室性心动过速及心室颤动。     

水飞蓟宾防治消化道肿瘤的研究进展

水飞蓟宾用于治疗肝脏疾病历史悠久,其抗氧化、抗纤维化、促肝细胞再生等多重药理作用已得到广泛认可,近年来发现水飞蓟宾在多种肿瘤模型中表现出抗肿瘤作用,此文就水飞蓟宾防治消化道肿瘤尤其是结直肠癌方面的研究进展进行综述.     

维甘苏胶囊治疗318例慢性乙型肝炎的临床小结

维甘苏胶囊是以菊科植物水飞蓟(Silybum marianum L.Gaertn)干燥果实中提取的治疗肝炎有效成分——水飞蓟宾制备的。其原植物产于南欧和北非,民间用于治疗肝胆疾病,国外学者H.Wagner等从中提取到水飞蓟宾——一种黄酮类化合物,经药理试验证明,对多种肝脏毒物引起的肝损伤均有明显的防护作用,临床研究证实其对急慢性肝炎有很好的治疗作用,德国已批准生产此药,商品名为“利肝隆”。目前水飞蓟宾已被公认为治疗肝炎的5大有效植物药物之一。我们从1995年8月～2000年8月用西安利君精华药业有限责任公司生产的维甘苏胶囊对418例慢性乙型肝炎患者进行了临床观察,结果如下。     

水飞蓟宾对实验兔球囊血管损伤后内膜增生的影响

探讨水飞蓟宾对兔球囊血管损伤后内膜增生的影响。将新西兰大白兔随机分为对照组 (n =6 )、小剂量水飞蓟宾组 [n =8,2 0mg (kg·d) ]、大剂量水飞蓟宾组 [n =8,4 0mg (kg·d) ]。用球囊导管对实验兔行髂动脉损伤 ,用药组于术前 3d分别用小剂量及大剂量水飞蓟宾 ,术后 2 8d取病变血管染色并免疫组织化学检查 ,以计算机图像分析系统分析血管内膜、中膜厚度和腔面积的变化 ,计算内膜增生细胞核抗原增殖指数。结果发现 ,小剂量水飞蓟宾对血管内膜和中膜厚度、腔面积、内膜增生细胞核抗原阳性细胞百分比无明显影响 (P >0 .0 5 ) ;大剂量水飞蓟宾使腔面积扩大、内膜厚度减少、内膜增生细胞核抗原阳性细胞百分比减少 (P <0 .0 5 )。提示水飞蓟宾能抑制血管内膜增生 ,有可能用于防治再狭窄。     

人参与电针对缺血性室颤的作用及其与M受体关系的实验研究

目的 探讨人参和电针刺穴位对缺血性室颤值的防治作用及其与M受体的关系。方法 实验用高位结扎冠状动脉前降支大鼠模型和直接刺激心室肌诱发室颤阈值测定的方法。结果 高位结扎冠状动脉前降支后大鼠室颤阈(VFT)明显降低,而人参或电针刺穴位可使VFT明显升高;缺血心肌对阿托品致颤作用处高敏状态,经人参或电针治疗后缺血心肌对阿托品致颤的耐受性明显升高;缺血心肌肉M-受体数量明显减少,反应性(kd值)明显增大,环磷酸鸟苷(cGMP)水平也明显升高,经电针治疗后缺血心肌内M-受体数量虽无变化,但kd值及cGMP水平均明显下降,接近正常水平。结论人参和电针对缺血性室颤有良好的防治作用,其机制部分与M受体的良性调制有关。     

水飞蓟宾治疗对非酒精性脂肪性肝病患者转氨酶影响的Meta分析

目的对水飞蓟宾治疗对非酒精性脂肪性肝病患者转氨酶影响的文献进行Meta分析,探讨水飞蓟宾对脂肪肝患者的护肝作用。方法计算机及手工检索知网、万方、维普网、Sinomed、Pubmed、Medline、Embase、ScienceDirect等数据库,收集关于水飞蓟宾治疗非酒精性脂肪性肝病患者的随机临床对照试验文献,根据纳入排除标准筛选后评价文献质量,并提取数据,采用RevMan 5. 3软件进行Meta分析。结果共纳入8篇文献,共计665例患者,在使用水飞蓟宾治疗8周～3个月后,可明显降低NAFLD患者血清ALT水平[加权均数差(WMD)=-11. 60,95%可信区间(95%CI):-18. 68～-4. 51,P=0. 001]和AST水平[WMD=-11. 56,95%CI:-16. 93～-6. 18,P 0. 001]。结论水飞蓟宾可明确降低非酒精性脂肪性肝病患者血清ALT、AST水平。     

鹿茸方对糖尿病肾病大鼠调钙蛋白(RGN) mRNA表达的调节

应用雄性Wistar大鼠腹腔注射链脲霉素诱导DN动物模型,造模成功后分为模型组、鹿茸方小剂量治疗组、鹿茸方中剂量治疗组、水飞蓟宾治疗组及正常对照组。干预治疗8周后,测定各组大鼠24小时尿微量白蛋白排泄量(UAER);用RT-PCR法测定各组大鼠RGN mRNA的表达。结果:模型组大鼠UAER显著增高、肾皮质RGN mRNA表达显著降低(P0.05);②治疗组显著降低模型UAER,显著上调肾皮质RGN mRNA的表达(P0.05);结论:鹿茸方及对照药物水飞蓟宾均对DN有一定治疗作用,其作用机制与上调肾皮质RGN mRNA的表达有关。     

电针及人参对慢性心肌梗死大鼠室颤阈（VFT）的影响

目的：探讨中药人参及针刺对心肌梗死诱发心律失常的良性调整作用,方法：采用结扎大鼠左冠状动脉前降支的慢性心肌梗死模型,用室颤阈（VFT）为观察指标,共选用SD纯种成年大鼠90只,体重200－250g,雌雄不限,随机分为正常组,假手术组,假手术电针组,结扎组,结扎＋电针组,结扎＋人参治疗组,电针组取“内关”“灵道”穴每天电针30分钟治疗2周,人参组以及人参水煎剂每日一次（1g/ml)喂养2周,结果：电针治疗组及人参治疗组慢性心梗大鼠室颤阈均显著高于未治疗组,并能改变缺血心肌对异丙肾上腺素的致颤敏感性,结论：电针及人参治疗能提高缺血心肌的室颤阈,降低其易颤性,及其对致颤药敏感性。     

The electrophysiologic effect of atenolol and nitrendipine on normal and ischemic rabbit myocardium in situ. III. Effects on ventricular fibrillation threshold

This study was designed to assess myocardial vulnerability by measuring ventricular pacing threshold (VPT), multiple extrasystoles threshold (MET), ventricular tachycardia threshold (VTT) and ventricular fibrillation threshold (VFT) by means of the pulse train stimulating method. The results showed that: (1) VFT is a quantitative index of myocardial vulnerability: (2) MET, positively correlated with VFT, might become a substitute for VFT as an index of vulnerability to ventricular fibrillation: (3) atenolol, both in normal and ischemic myocardium, is able to make a significant elevation of VFT, which is considered as an antifibrillation effect: (4) nitrendipine exerted no apparent effects on all the parameters.     

Effects of calcium channel agonism by Bay-K-8644 on ventricular fibrillation threshold of isolated heart

Summary The hypothesis tested was that enhanced entry of calcium into cardiac cells would increase the susceptibility to ventricular fibrillation as measured by the ventricular fibrillation threshold (VFT) of the isolated perfused rat heart. Bay-K-8644 was used as a calcium-channel agonist. There was a biphasic effect with a maximal increase in left ventricular systolic pressure and oxygen uptake at a concentration of 10^-7M. The same concentration caused a major reduction in the VFT. The bell-shaped pattern of fall of the VFT was inversely related to the effect on LV developed pressure. The changes in VFT could be dissociated from those on myocardial metabolites. Although Bay-K-8644 increased the heart rate, reduction of the VFT could also be obtained in paced hearts. The addition of ryanodine, an agent known to interrupt intracellular recycling of calcium through the sarcoplasmic reticulum, was able to abolish approximately half the effect of Bay-K-8644 on the VFT. Therefore, increased entry of calcium via the calcium channel is able to reduce VFT, acting in part through enhanced recycling of calcium through the sarcoplasmic reticulum.     

Prevention of cardiac fibrillation using antioxidants and preliminary adaptation of animals to the effects of stress

Electrical ventricular fibrillation threshold (VFT) was determined, using programmed isolated stimuli on the left-ventricular apex, in male Wistar rats at different times after 10 hours' immobilization stress (IS). The VFT decrease reached a maximum of 48% 12 hours after IS. Cardiac sensitivity to the inhibiting vagal influence was increased considerably at the same time. The adaptation to short episodes of IS over 6 days, intermittent exposure to high-altitude hypoxia (5 hours daily at a 5000 m "altitude" for 40 days) and the antioxidant ionol (50 mg/kg) prevented IS-induced fibrillation threshold decrease. In cases of coronary arterial ligation in waking animals, the antioxidant ionol reduced fourfold the mortality associated with ventricular fibrillation and raised the spontaneous defibrillation rate from 28% to 72%. Possible mechanisms of these phenomena are discussed.     

奎尼丁与胺碘酮对犬心室复极和室颤阈值影响的比较

采用记录心外膜单相动作电位和电刺激技术观察口服奎尼丁或胺碘酮4周后的犬心室电生理参数的改变,以探讨奎尼丁和胺碘酮对犬心室电生理效应的影响。结果显示:奎尼丁和胺碘酮延长心室有效不应期分别达42.2%和51.9%(P 均<0.01),延长 Q-T 间期分别达58.1%和62.4%(P 均<0.01)。奎尼丁延长 QRS 时限达47.9%(P<0.01),其延长单相动作电位复极50%～90%Ⅱ寸程(MAPD_(50～90))较胺碘酮更显著(P<0.01),并使其复极离散度(MAPDd)增加105.9%(P<0.01),对室颤阈值(VFT)无显著影响。而胺碘酮延长 QRS 时限无统计学意义(P>0.05),对 MAPDd 无显著影响,提高 VFT 达52.0%(P<0.01)。实验表明胺碘酮能提高心室电稳定性而奎尼丁无助于心室电稳定性的提高。     

左室后负荷的改变对心室颤动自限性的影响

目的采用在体兔心脏模型研究左室后负荷的改变对心室颤动(VF)自限性的影响。方法采用自制主动脉缩窄夹机械性地部分夹闭主动脉根部,分级增加左室后负荷;使用PFA-05型输液泵控制性输注硝普钠,通过分级减小左室后负荷;测定a(左室前壁)、b(左室心尖部)两部位的心室舒张期阈值(VDT),心室相对不应期(VRRP),心室有效不应期(VERP),不应期离散(RPd),心率,左室压力,随后,用脉冲串刺激诱发VF,观察诱发VF的致颤阈值(VFT)。结果在在体兔心脏模型,增加左室后负荷,VRRP、VERP、VFT较夹闭前明显降低(P<0.05或P<0.01),但RRPd、ERPd较夹闭前明显升高(P<0.05或P<0.01);减小左室后负荷,上述参数无明显变化(P>0.05)。结论增加左室后负荷,心室的不应期缩短,其离散度增大,VFT下降,VF易诱发。     

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.     

Ventricular fibrillation threshold measured by continuous 50 cps stimulation for the evaluation of the antifibrillatory effect of the drugs

The role of electrophysiologic parameters on the induction of ventricular fibrillation (VF) by continuous 50 cycle per second (cps) electrical stimulation was studied in 21 open chest dogs. The current strength of the 50 cps stimulation required to induce VF when applied to the ventricle for 2 seconds was defined as the ventricular fibrillation threshold (VFT). The intravenous injection of antiarrhythmic drugs raised the VFT in a dose dependent manner. The changes in VFT were associated with a rise in excitation threshold. The slopes of the regression equations relating the excitation threshold to VFT were almost identical, that is, 2.8 with lidocaine, 3.4 with procainamide and 3.2 with disopyramide. Prolongation of refractory period increased the cycle length of ventricular excitations just prior to VF but was not correlated with the changes in VF. Localized myocardial ischemia induced by coronary ligation also resulted in the elevation of VFT. The slope of the regression equation between excitation threshold and VFT was 1.9 which was slightly lower than that observed at the administration of the drugs. The fact that the VFT was mainly attributed to the changes in excitation threshold at the site where the test stimulus was applied would limit the usefulness of the 50 cps continuous stimulation method for the evaluation of vulnerability to VF.     

The effect of disopyramide phosphate on ventricular fibrillation threshold of normal and ischemic ventricles

The effect of disopyramide phosphate (DP) infusion (1 mg/Kg and 2 mg/Kg BW) on ventricular fibrillation threshold (VFT) was studied in anesthetized dogs. In the 1 mg/Kg group, the VFT increased 47% above the control level immediately after infusion. In the 2 mg/Kg group, a delayed increase in VFT was observed after the initial period and VFT was not correlated with the plasma concentration of DP. This phenomenon was abolished by pretreatment with methacholine. These results suggested an anticholinergic action of DP on the VFT. In the ischemic dogs produced by acute coronary occlusion, DP prevented a decrease in VFT.     

Antiarrhythmic effect of cardiac sympathectomy

The authors studied the effect of sympathetic denervation of the heart (removal of the stellate ganglion together with the sympathetic trunk up to the level of the 5th thoracic ganglion) on the ventricular fibrillation threshold (VFT) in dog. The acute experiments were performed under general anaesthesia with pentobarbital. Unilateral left sympathetic denervation raised the VFT to 144% of the initial value (14 measurements) and unilateral right sympathectomy to 214% (9 measurements). Immediately after bilateral denervation the VFT increased to 242% (23 observations). Atropine blockade of the vagus nerve (0.1 mg/kg b.w.) displayed no effect on the VFT increase. The observed increase in VFT corresponded with the finding that bilateral sympathetic denervation of the heart protected the dogs from spontaneous ventricular fibrillation after ligating the intraventricular branch of the left coronary artery. The authors compared their own results with those reported in the literature and discuss the possible clinical use of sympathetic denervation of the heart in the treatment of tachyarrhythmia.