脂质体携载L-Arg对Wister大鼠心肌钙负荷的影响

The Effect of Liposomes Carrying L-Arg on Wister Rat′s Cardiomyocytes Calcium Load.

目的探讨NO对心肌钙负荷的影响。方法脂质体包裹L-Arg离体灌注雄性Wistar大鼠心脏模型,观察心肌钙负荷及相关损害指标的变化。结果脂质体包裹L-Arg组促进心肌细胞cGMP合成,并明显降低I/R心肌钙含量和45Ca2+内流,抑制心肌蛋白漏出;与I/R损伤组比较,L-NNA灌流,明显增加心肌钙含量(P<0.05)和Ca2+内流(P<0.01),心肌cGMP降低50%(P<0.05),心肌蛋白漏出增加26.53%(P<0.05);L-Arg脂质体的作用可被L-NNA所逆转。结论L-Arg导入心肌细胞,可以改善缺血心肌的NO缺陷,抑制Ca2+内流,拮抗氧自由基,进而发挥细胞保护作用。

Objective To discuss the effect of cardiac muscle calcium load on nitric oxide. Methods Liposomes carrying L - Arg was perfused into male Wister rat＇s heart modelaorta in vitro, so that we observed cardiac calcium load and correlative injure idexes. Results Liposomes carrying L -Arg promotd cGMP production in cardiomyoeytes, and markedly decreased I/R calcium load as well as^45 Ca^2＋ inner flow,and inhibited cardiac muscle protein leakage. As compared with I/R injure group, L- NNA profuing could increase cardiac calcium content （P 〈0.05） and Ca^2 ＋ inner flow markedly（P 〈0. 01）. Cardiac muscle cGMP decreased by 50% （P 〈 0.05） ,and leakage of cardiac muscle protein increasesd by 26.53% （ P 〈 0.05 ）. The role of liposomes carrying L - Arg may be reversed byL - NNA. Conclusion L - Arg entering cardiomyocytes may improve NO production and function defect of ischaemia or I/R injure cardiac muscle,and inhibit cardiac muscle Ca^2＋ inner flow and weaken free radicel,so that play cell protective function.