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本工作在离体灌流的大鼠心脏缺血-再灌注(I/R)损伤模型上,观察了脂质体携载L-精氨酸(L-Arg)的保护作用。结果发现,1mol/L L-Arg脂质体灌流心脏,明显抑制缺血心脏再灌注时心肌MDA含量和线粒体Ca~(2+)含量的增加,显著减少心肌细胞内的酶(乳酸脱氢酶、组织强白酶D)和肌红蛋白的漏出及心肌MDA的释放,明显增加冠脉流量。而相同剂量的游离L-Arg则无明显保护效应。我们在离体大鼠灌流的主动脉条上进一步发现,L-Arg脂质体具有显著的血管舒张效应。而游离L-Arg则不具有明显舒张效应。结果表明,脂质体作为药物载体,包裹内源性EDRF释放剂防治心肌I/R损伤是有效的。可能具有临床应用前景。
This study was designed to observe the protective effects of L-arginine (L-arginine) on liposomes in a rat model of myocardial perfusion induced by ischemia / reperfusion (I / R) injury. The results showed that 1mol / L L-Arg liposome perfusion of the heart, myocardial ischemia reperfusion significantly decreased myocardial MDA content and increased content of mitochondrial Ca2 +, significantly reduce myocardial enzymes (lactate dehydrogenase , Organization of strong enzyme D) and myoglobin leakage and myocardial MDA release, significantly increased coronary flow. The same dose of free L-Arg no significant protective effect. We further found in the aortic strips perfused in vitro that L-Arg liposomes have a significant vasodilatory effect. The free L-Arg does not have significant relaxation effect. The results showed that liposomes as a drug carrier, wrapped endogenous EDRF release agent to prevent myocardial I / R injury is effective. May have clinical application prospects.