Rodent model of renal ischemia and reperfusion injury: influence of body temperature, seasonal variation, tumor necrosis factor, endogenous and exogenous antioxidants.

The influences of body temperature (T), seasonal variation, antiserum of tumor necrosis factor (TNF), exogenous and endogenous antioxidants on the extent of renal injury in a rodent model were examined. Renal injury was induced by 15-45 min of renal vascular (arterial and venous) occlusion followed by 1-3 days of reperfusion in right-nephrectomized male rats. Plasma creatinine concentration (PC, a reflection of renal injury) was independent of T when T was within 35-40 degrees C (n = 8), but directly related to T when T was within 31-35 degrees C (n = 10). PCs in rats with renal insults performed during October, November and December were similar (600 mcM, n = 10-24), but were higher than that during April (380 mcM, n = 16). Neither TNF antiserum nor exogenous antioxidants (Trolox, ascorbic acid, phytic acid, U-78517F) reduce PC (n = 5-7). However, PC was lower in normal rats than vitamin E deficient rats when subjected to 45 min (329.1 +/- 93.6 mcM vs. 695.9 +/- 37.7 mcM, n = 5-6), but not to 15-30 min of ischemia. In conclusion, renal injury induced by ischemia/reperfusion was T- and season-dependent. An excess of exogenous antioxidants did not reduce, whereas a reduction in endogenous antioxidant vitamin E level enhanced, renal injury.