大鼠心脏缺血-再灌注损伤对心肌L-Arg/NO途径的影响

为探讨大鼠心脏缺血-再灌注损伤(IRI)期间一氧化氮(NO)生成增加的环节和过程。本实验用离体灌流大鼠心脏,预灌流15 min,停灌45 min,取30 ml KH 液循环灌流15 min,观察冠脉流出液中细胞胞浆酶(LDH)、蛋白质、肌红蛋白漏出量和NO

Effects of myocardial ischemia reperfusion injury on L-arginine/nitric oxide system in rat heart

Ischemia reperfusion injury (IRI) model of rat heart was prepared by preperfusion for 15 min, then a suspension for 45 min and recycling reperfusion for 15 min with 30 ml KH buffer. The leakage of lactate dehydrogenase(LDH),protein, myoglobin and nitrite (NO2-) in the circular perfusion fluid were measured. Myocardial nitric oxide synthase(NOS) activity and L-arginine transport were observed. In the IR group, the leakage of LDH,protein, myoglobin and NO2- were increased respectively by 4.1,5.4,1 and 1.2 times(P<0.01) and NOS(tNOS, iNOS, cNOS) activity by 48.2%,43.2% and 52.1%,(P<0.01,respectively) as compared with the control group. L-arginine transport might be mediated by either high- or low-affinity transport system in cardiac tissue. In the IR group, L-arginine transport increased significantly with the V(max) being increased by 48% and 2 times respectively for the low-affinity and the high-affinity transport as compared with control. Michaelis constant (km) was decreased by 47.4% for low-affinity transport (P<0.05),but not significantly changed for the high-affinity transport. These results suggest that the increase of nitric oxide generation might result from the increased myocardial NOS activity and L-arginine transport during IRI.