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作 者:李红[1] 牛欣[1] 李国彰[1] 施雪筠[1] 魏执真[2] 肖俊平[1] 孙秀华[1] 吴秉芹[1] 薛明[1] 席时芳[1]
机构地区:[1]北京中医药大学,北京100029 [2]北京中医医院,北京100010
出 处:《中国中药杂志》2006年第9期759-762,共4页China Journal of Chinese Materia Medica
摘 要:目的:研究调脉饮注射液的抗实验性心律失常作用,并初步探讨其作用机制。方法:动物随机分为空白对照组、阳性药对照组和调脉饮注射液大、小剂量组,观察:对小鼠吸入氯仿所致室颤的保护作用;大鼠经20%乌拉坦6 mL.kg-1静脉麻醉后开胸,从颈静脉匀速滴入1.0μg.mL-1.min-1乌头碱溶液,豚鼠麻醉后从颈静脉匀速滴入10μg.mL-1.min-1哇巴因溶液,观察出现室性期前收缩、室性心动过速、室颤和心搏停止的时间,然后换算为乌头碱和哇巴因的累积量;大鼠麻醉后开胸,结扎冠状动脉5 min后恢复冠脉供血,造成缺血再灌注,观察心律失常持续时间。实验结束后取心脏制成10%匀浆,测定超氧化物歧化酶(SOD)和丙二醛(MDA)含量。结果:调脉饮注射液可以提高室颤阴性率,降低小鼠室颤的发生率(P<0.01);推迟大鼠室性早搏、室速及室颤的发生时间,提高乌头碱的累积用量,具有抗乌头碱心律失常(P<0.05)的作用;推迟豚鼠室性早搏的发生时间,提高哇巴因的累积用量,具有抗哇巴因心律失常(P<0.05)的作用;对心肌缺血再灌注所致心律失常有保护作用,能够缩短心律失常的持续时间,并能明显提高心肌SOD的活性。结论:调脉饮注射液能对抗实验性心律失常,对心肌缺血再灌注所致心律失常有保护作用,其作用机制可能与抑制脂质过氧化,减少自由基损伤有关。Objective: To study the effect of Tiaomaiyin injection on the experimental arrhythmia for analyzing its tmderlying mechanism in the treatment of cardiovascular disease. Method: Experimental animals anesthetized with 20% urethane (6 mL·kg^- 1 ) were evenly randomized into control group, positive control group, low-dose and high-dose Tiaomaiyin group. The rate of ventricular fibrillation (VF) chloroform-induced in mice, and the epoch of ventricular extrasystole (VE), ventricular tachycardia (VT),VF and cardiac arrest (CA), actonitine-induced in rats (1.0μg·mL^-1·min^-1), and vabain-induced in guinea pigs (10μg·mL^-1·min^-1), were detected respectively. The result loas converted into cumulative dosage of actonitine or vabain. In ischemia-reperfusion model in rats, the duration of arrhythmia and activity of superoxide dismutase(SOD) and malondialdehyde (MDA) were detected. Result: After venous injection of Tiaomaiyin, VF in mice was lower significantly (P 〈 0.01), VE, VT, VF in rats and VF in guinea pigs were lowered considerably (P 〈 0.05). The duration of arrhythmia in ischemia-repeffusion model was reduced considerably (P 〈 0.05), and the activity of myocardial SOD was raised significantly (P〈 0.01). Conclusion: Tiaomaiyin shows the reduction of experimental arrhythmia and protect effect to ischemia-reperfusion injury of the heart, which indicates that the effect mechanism may have the relationship with inhabition of lipid peroxidation and damnification of the free radical.
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