地奥心血康对心肌缺血再灌注损伤的抗脂质过氧化作用的研究

目的:揭示地奥心血康(DK)对心肌缺血再灌注损伤的抗氧化作用与机制。方法:用成年杂种犬复制心肌缺血再灌注损伤模型。多道生理记录仪监测心功能指标;酶法测定AST、CK、LDH含量;荧光法测血清与心肌细胞膜MDA含量;电子自旋共振(ESR)记录微分谱线进行体外羟自由基捕捉实验。结果:①生理盐水对照(NS)组随着缺血再灌注时间的延长,LVSP,±dp/dt_max呈进行性下降;而DK组缺血再灌注后LVSP和±dp/dt_max虽有下降,但显著高于NS组(P＜0.05);②血清中AST,CK,LDH含量随缺血/再灌时间延长均增高,于再灌120min后DK显著低于NS组(P＜0.05);③血清MDA含量于再灌注240min时DK组显著低于NS组(P＜0.05);④DK组心肌细胞膜MDA含量也显著地低于NS组(P＜0.05);⑤在DK浓度为0.71%、1.43%和2.14%时,羟自由基强度分别减少66%、80%和100%。结论:DK对心肌缺血再灌注损伤犬的心功能和心肌细胞膜有明显的保护作用,其很强的清除羟自由基的功能是实现这种保护效应的重要机制。

Di-Ao-Xin-Xue-Kang''''s anti-peroxide protective effect against myocardial ischemia-reperfusion injury

AIM: To investigate the protective effect and mechanisms of di-ao-xin-xue-kang (DK) on myocardial ischemia-reperfusion. METHODS: Models of myocardial ischemia-reperfusion were constructed with sixteen mongrel dogs. The left ventricular pressure (LVSP), the marximal/minimum rate of LVSP (±dp/dt_max) and the serum aspartate aminotransferase (AST), creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA) were determined before and 90 minutes after occlusion, 120 and 240 minutes after reperfusion, and the MDA content in myocardial cell membrane prepared at 240 minutes after reperfusion was determined. The oxygen free radical was assayed with electron spin resonace spectroscopy (ESR) technique. RESULTS: ① LVSP and ±dp/dt_max in the normal saline control (NS) group decreased with the time progress of occlusion-reperfusion, and it was the same in DK group, but the levels were significantly higher than that in NS group (P＜0.05). ② The serum AST, CK, LDH contents increased with the time progress of occlusion-reperfusion in the both groups, but in DK group the levels at 120 and 240 minutes after reperfusion were markedly lower than that in NS group (P＜0.05). ③ The serum MDA level at 240 minutes after reperfusion in DK group was significantly lower than that in NS group (P＜0.05). ④ The MDA level in myocardial cell membrane in DK group was significantly lower than that in NS group (P＜0.05). ⑤ The hydroxyl radical intensity was reduced by 66%, 80% and 100% under the DK concentration of 0.71%, 1.43% and 2.14%. CONCLUSION: DK significantly reduces the production of lipid peroxide in myocardial ischemia-reperfusion, and the scavenging of hydroxyl radical is an important mechanism.