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

Methods Find Exp Clin Pharmacol. 1993 Apr;15(3):153-9.

Abstract

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.

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Body Temperature / physiology*
  • Creatinine / blood
  • Ischemia / physiopathology*
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Renal Circulation / physiology*
  • Reperfusion Injury / physiopathology*
  • Seasons*
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism*
  • Vitamin E Deficiency / physiopathology

Substances

  • Antioxidants
  • Tumor Necrosis Factor-alpha
  • Creatinine