[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.
Zheng
H Z
HZ
Department of Physiology, Guangdong Medical College, Zhanjiang  524023.
Tang
C S
CS
Su
J L
JL
Wu
T
T
D000818:Animals; D001120:Arginine / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism; D005260:Female; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D051381:Rats; D017208:Rats, Wistar
D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D006152:Cyclic GMP