Objective: This study aimed at evaluating whether supplementation of L-arginine in the course of ischemia and reperfusion syndrome after acute, experimental ischemia of the hind legs of the rat, could influence nitric oxide (NO) concentration and selected biochemical parameters concentration related to the oxidative stress.
Material and methods: The study included 64 male Wistar rats. The animals were divided into four groups: Group I = control, Group II = placebo, Group III = L-arginine (500 mg/kg body mass/day for 5 days, p.o.), Group IV = L-arginine and nonspecific nitric oxide synthase (NOS) inhibitor - N(G)-Nitro-L-arginine-methyl ester (L-NAME) (75 micromol/ rat/day for 5 days, p.o.). Each group was further divided into subgroups: 1 = animals not subjected to ischemia and reperfusion, 2 = animals underwent 4-hour ischemia and subsequent reperfusion. Animals from Subgroup 2 were anesthetized and submitted to acute tourniquet ischemia of the hind limb. Blood samples were collected from all anesthetized rats by puncturing the right ventricle to assess total antioxidant status, lipids' peroxide concentration and nitric oxide concentration before ischemia and at 4th hour of ischemia and at 30th, 60th or 120th minute of reperfusion.
Results: We found that administration of L-arginine to rats resulted in significant increase of NO, level of total antioxidant status (TAS), and decrease of lipid' peroxide concentration when compared to the control and placebo groups. All these laboratory changes were progressing along with lengthening of reperfusion time. Simultaneous application of L-NAME led to reversal of phenomena caused by L-arginine.
Conclusions: The present results suggest that L-arginine may protect tissues and organs against ischemia-reperfusion injury. The potential therapeutic role of L-arginine administration in prevention and treatment of ischemia-reperfusion syndrome consequences needs further investigation in humans.