The Effect of O2 Radical Scavenger (SOD) and Intrarenal Calcium Membrane Blocker (verapamil) in the Renal Function Following Warm Ischemia

Lee, Ahn Kie; Kim, Si Whang

Abstract

During renal ischemia, ATP is degraded to hypoxanthine. When xanthine oxidase converts hypoxanthine to xanthine in the presence of molecular oxygen, superoxide radical (O2) is generated. This is toxic to cellular membranes through lipid peroxidation and may play an important role in the ischemic damage of the kidney. At the cellular level, with reperfusion there is accumulation of calcium and this potentiates oxygen free radical injury. The purpose of the present study is to determine whether oxygen free radicals and calcium play a role in mediating injury after renal ischemia. The ability of oxygen free radical scavenger (SOD) and calcium membrane blocker (verapamil) to protect renal function in the rabbit after renal ischemia was determined. The New-Zealand white rabbit was explored and occluded both renal arteries for 60 minutes with microvascular clamps. Group 1 (n=7) had normal saline infused into the both renal arteries followed by 60 minutes ischemia, group 2 (n=5) had SOD (10mg/kg) infused into the both renal arteries just before clamping, group 3 (n=5) had verapamil 15mg/kg infused. The results were as follows. Plasma creatinine in the group 2(1.7+/-0.1 mg/dl) was lower than group 1 (2.6+/-0.2 mg/dl) (p<0.05). Creatinine clearance and Ucr/Pcr in the group 2 (4.8+/-0.2ml/min, 19.8+/-2.6) was higher than group 1 (1.5+/-0.1 ml/min, 19.8+/-2.6) (p<0.05). Urine osmolarity in the group 2(574.6+/-22.3 m Osm/kg) was higher than group 1 (342.27+/-84.7 m Osm/kg). The function of solute handling was more reserved in the group 2 than group 1. (FeNa+ of group 1 vs. group 2 ; 6.9+/-0.6, vs. 2.0+/-0.3) (p<0.05). There was no difference between group 1 and 3 except Ccr. From these observations we conclude that free radical scavengers provide significant protection from the injury to the kidney and increased intracellular calcium potentiates renal injury during reperfusion.