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作 者:李俊[1] 廖雪珍[2] 廖慧芳[2] 苏宁[2] 黄桂英[2] 张春红[3] 冯少华[3] 周才杰[3] 王帅[3]
机构地区:[1]广东省中医院急诊科,广东广州510120 [2]广州中医药大学中药学院药理教研室,广东广州5100006 [3]广州中医药大学中药学院,研究生广东广州510006
出 处:《广州中医药大学学报》2008年第6期519-521,共3页Journal of Guangzhou University of Traditional Chinese Medicine
摘 要:【目的】观察暖心胶囊对腹主动脉狭窄诱导心衰模型大鼠的影响。【方法】选用SD大鼠40只,采用腹主动脉狭窄诱导法复制心衰大鼠模型,造模成功大鼠随机分为模型组,暖心胶囊低、高剂量组(剂量分别为0.825、1.650 g.kg-1.d-1),地戈辛组(剂量为0.091 m.gkg-1·d-1),并设假手术组对照;检测各组大鼠心率(Rheart)、外周收缩压(pSB)、外周舒张压(pDB)、左室收缩压(pLVS)、左室舒张末压(pLVED)、左室内压上升/下降最大速率(V±dp/dt)、血清超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量。【结果】低、高剂量暖心胶囊可升高模型大鼠pSB、pLVS、V±dp/dt,降低pLVED,增加SOD活性,降低MDA含量,与模型组比较有显著性差异(均P<0.05),并可不同程度减慢心率,但与模型组比较无显著性差异(P>0.05)。【结论】暖心胶囊治疗心衰的作用可能与其能改善心脏收缩与舒张功能,纠正体内自由基代谢紊乱,抑制心肌脂质过氧化有关。Objective To observe the effect of Nuanxin Capsule (NC) on rats heart failure (HF) induced by abdominal aorta constriction. Methods Rat models of HF were induced by the method of abdominal aorta constriction. Then the HF rats were randomized into the model group, NC groups (treated with NC at 0. 825 and 1. 650 g·kg^-1·d^-1 respectively), and digoxine group (digoxine at the dose of 0. 091 mg·kg^-1·d^-1 ). Meanwhile, the pseudo-operation group was established. After treatment for 30 days, the heart rate, systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal rate of increase and decrease in left ventricular pressure ( ± dp/dt) as well as levels of serum superoxide dismustase (SOD) and malondialdehyde (MDA) were measured. Results High- and low-dose NC increased SBP, LVSP and ± dp/dt, decreased LVEDP, increased SOD activity, and reduced MDA content, the difference being significant as compared with the model group (P 〈 0. 05). NC also slowed heart rate, but the difference was insignificant ( P 〉 0. 05 compared with that in the model group ). Conclusion The therapeutic mechanism of NC for heart failure is probably related with the improvement of cardiac systolic and diastolic function, and with the regulation of free radical metabolism and the inhibition of myocardial lipid peroxidation.
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