The clinical potential of free radical (OFR) ablative therapy is dependent upon the proportion of the total injury caused by the reperfusion mechanism compared with the proportion resulting from ischemic injury itself. Prostaglandin cascade can both activate and be activated by OFR.
Aim: to investigate the influence of different periods of cold ischemis in renal tissue (cortex and medulla) -regarding superoxide dismutase (S.O.D.) activity, the amount of erythrocyte trapping and prostaglandin synthesis. Also, to evaluate the effect of exogenous S.O.D. in the prevention of reperfusion injury.
Material and methods: 48 Lewis male rats (200-250 g) received renal isografts (RTx) preserved in Collins solution at 4 C for different periods: control group (8) non operated; group I (8) immediate RTx; group II (8) 12 hrs; group III (8) 18 hrs; group IV (8) 12 hrs+S.O.D. (13 mg/kg e.v.); group V (8) 18 hrs+S.O.D. (13 mg/kg e.v.). Before reperfusion all recipients received 1 ml of 51-Cr labelled erythrocytes. After 15 min. reperfusion grafts were removed and samples (cortex and medulla) obtained for measuring trapping of erythrocytes. S.O.D. activity and prostaglandins (PGe2, TxB2, 6-Keto-PGF1).
Results: A strong correlation was found between the duration of cold ischemia and the amount of trapping both in cortex and in medulla. S.O.D. administration induced a significant drop of trapping. In non-operated rats S.O.D. activity in cortex was two fold medulla content. However, after reperfusion, a significant decrease in cortex was found in all groups. S.O.D. administration raised S.O.D. activity in cortex similar to control values.(ABSTRACT TRUNCATED AT 250 WORDS)