环维黄杨星D抗异丙肾上腺素致心肌缺血药理研究

目的:探讨环维黄杨星(Cvb-D)抗异丙肾上腺素致心肌缺血的药理作用和可能机理。方法:给大鼠灌服0.55、1.1和2.2 mg/kg Cvb-D,连续21 d,通过制备异丙肾上腺素诱发的心肌缺血性模型,观察各组大鼠的ECG、血清CPK、LDH活性、FFA含量及心肌组织中SOD的活性和脂质过氧化产物MDA的含量。结果:Cvb-D可显著减少心肌缺血性模型大鼠∑J,缩短ECG恢复时间;显著降低心肌缺血性模型大鼠血清中FFA含量;显著降低心肌缺血性模型大鼠血清中CPK、LDH活性;降低心肌缺血性模型大鼠心肌组织的MDA含量,升高心肌缺血性模型大鼠心肌组织SOD活性。结论:Cvb-D具有抗异丙肾上腺素致心肌缺血药理作用,其降低血清FFA、CPK、LDH水平、改善心肌MDA及SOD活性是Cvb-D的抗心肌缺血作用机理。

A Pharmacology Study of Cyclovirobuxinum D on Curing Myocardial Ischemia Induced by Isoprenaline

OBJECTIVE: To explore the pharmacology actions of Cyclovirobuxinum D (Cvb-D) for the myocardial ischemia and study its possible mechanism. METHODS: The rats were given orally with Cvb-D 0.55 g/kg, 1.1 g/kg and 2.2 g/kg per day, for 21 days. The myocardial ischemia model were induced by isoprenaline. The rats ECG, serum CPK, LDH, FFA and myocardium tissue SOD, MDA level were detected. RESULTS: Cvb-D could significantly reduce myocardial ischemia model induced by isoprenaline rats' sigmaJ of ECG, shorten ECG resume time, reduce serum FFA content, serum CPK, LDH activation, reduce cardiac tissue MDA content, raise the cardiac tissue SOD activation. CONCLUSION: Cvb-D can decrease the release of FFA, CPK, LDH and improve the model rats' myocardium MDA, SOD level. It may be some of mechanisms of its anti-myocardial ischemia effect.