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出 处:《内蒙古农业大学学报(自然科学版)》2014年第5期6-11,共6页Journal of Inner Mongolia Agricultural University(Natural Science Edition)
基 金:内蒙古自治区卫生厅重点课题
摘 要:本文研究蒙药匝迪对于大鼠快速型心律失常模型的药理作用及其对于Connexin43缝隙连接蛋白的表达的影响,探讨匝迪抗心律失常的作用及分子机制。将健康成年Wistar大鼠70只,随机分为7组,分别是:空白对照组,氯化钙诱发的心律失常模型对照组,氯化钙诱发的心律失常匝迪高、中、低剂量治疗组,以及乌头碱诱发的心律失常模型对照组,乌头碱诱发的心律失常匝迪治疗组。以氯化钙诱发和乌头碱诱发造模;造模成功后各治疗组以相应剂量匝迪水提液灌胃,连续10d。应用动物心电图机、心电示波器观察大鼠心电变化及对实验性心律失常的作用,应用免疫组化技术观察Connexin43(Cx43)缝隙连接蛋白的表达的变化。结果表明匝迪治疗组能够明显降低实验性心律失常大鼠的心率、延长P-R间期、Q-T间期(P<0.05);匝迪治疗组与其相应的模型对照组相比,心律失常的发生率和死亡率显著下降(P<0.05)。匝迪治疗组Cx43缝隙连接蛋白表达水平高于相应的模型对照组(P<0.05)。匝迪水提液能够减慢大鼠心率、延长P-R间期、Q-T间期,这一负性频率、负性传导作用可能是匝迪水提液抗心律失常作用的药理学基础,匝迪水提液可以增强实验性心律失常大鼠Cx43缝隙连接蛋白的表达,保持离子稳定和细胞间耦联,保持心肌传导的均匀,为其可能的作用机制。This thesis is to explore the pharmacological effects of Mongolian medicine Zadi on the arrhythmia model of rats and the effects on Connexin 43 expression;and to discuss its antiarrhythmic effects and molecular mechanism. In the experiment, 70 healthy adult Wistar rats were randomly divided into 7 groups, respectively. They are : a control group ; a model group of arrhythmias induced by calcium chloride, groups of arrhythmias induced by calcium chloride and treated with Zadi respectively in large dose, in medium dose and in small dose;the group of arrhythmia induced by aconitine, the group of arrhythmia induced by aconitine and treated with Zadi. First, models were induced by calcium chloride and aconitine. And then after modeling, each group was treated by intragastric administration of corresponding doses of the aqueous extract of Zadi for ten consecutive days. In the meanwhile, animal ECG, ECG oscillograph were applied to observe changes of ECG in rats and the effects of Zadi on experimental arrhythmia; immunohistochemical technique was used to observe the change of Connexin43 (Cx43) expression. As the result of the experiment, in the Zadi treatment groups the heart rate of rats with experimental arrhythmia could be significantly reduced, and the P - R interval and Q - T interval were prolonged ( P 〈 0. 05 ). Compared with the model group, the incidence and mortality of cardiac arrhythmia was significantly de- creased in the groups of Zadi treatment( P 〈 O. 05 ). And also in the groups of Zadi treatment, the Cx43 expression level was higher than that in the model groups( P 〈 0. 05 ). In conclusion, the aqueous extract of Zadi can slow down the heart rate in rats, and pro- long the P - R interval and the Q - T interval. This negative frequency and negative condution effects may be the pharmacological ba- sis of antiarrhythmic activity of the aqueous extract of Zadi. The aqueous extract of Zadi can enhance Cx43 expression, maintain ion stability and intercellular coupling, and maintain my
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