[Participation of the L-arginine-NO system in liver reperfusion injuries].

The L-arginine--NO system functioning in rabbits with hepatic ischemia and reperfusion was modified by infusing the NO synthase (NOS) inhibitor NG-nitro-L-arginine (15 mg/kg) or the NOS substrate L-arginine (300 mg/kg). The effect was evaluated by determining the lipid peroxidation (LPO) products (conjugated dienes, Schiff bases) and antioxidant system factors (alpha-tocopherol, retinol, catalase activity factor). The degree of reperfusive damage was evaluated by the alanine amino transferase (AlAT) and aspartate amino transferase (AsAT) activity in the blood of experimental animals. The development of ischemia and reperfusion leads to a significant growth in the LPO rate, depletion of the antioxidant system factors in the blood and liver tissue, and increase in the AlAT and AsAT activity. The L-arginine infusion prior to the reperfusion period decreased violation of the prooxidant-antioxidant state and favored normalization of the AlAT and AsAT activity in the blood. No such effects were observed as a result of the NOS inhibition prior to the onset of ischemia.