Attenuation of renal ischemia-reperfusion injury by FR167653 in dogs

Surgery. 2002 Jun;131(6):654-62. doi: 10.1067/msy.2002.124629.

Abstract

Background: Inflammatory cytokines are known to contribute to ischemia-reperfusion injury. We investigated the effect of FR167653 (FR), a suppressor of interleukin-1beta and tumor necrosis factor-alpha, on ischemia-reperfusion injury of the kidney in dogs.

Methods: The left kidney was subjected to ischemia for 60 minutes followed by removal of the right kidney. A control group (n = 10) and an FR group (n = 8) were evaluated for tissue blood flow; resistive index, pulsatility index, arterial oxygen pressure, serum creatinine, blood urea nitrogen, aspartate transaminase, and alanine transaminase levels; interleukin-1beta messenger RNA expression in the peripheral blood; apoptotic index; and histopathology.

Results: The FR group showed lower creatinine, serum urea nitrogen, aspartate transaminase, and alanine transaminase levels (P <.038 each) and lower interleukin-1beta mRNA expression and apoptotic index (P <.041 each) than did the control group. Arterial oxygen pressure during the 120 minutes after reperfusion in the FR group decreased but recovered quickly (P =.024). Renal tissue damage in the FR group was less than that in the control group (P =.036).

Conclusions: FR ameliorates ischemia-reperfusion injury of the kidney potentially by reduced production of inflammatory cytokines that may contribute to damage to the ischemic kidney and the distant organs.

MeSH terms

  • Animals
  • Apoptosis
  • Dogs
  • Female
  • Interleukin-1 / antagonists & inhibitors
  • Interleukin-1 / metabolism
  • Ischemia / drug therapy*
  • Ischemia / pathology
  • Ischemia / physiopathology
  • Kidney / pathology
  • Kidney / physiopathology
  • Lung / pathology
  • Lung / physiopathology
  • Male
  • Pyrazoles / therapeutic use*
  • Pyridines / therapeutic use*
  • Renal Circulation / drug effects*
  • Reperfusion Injury / drug therapy*
  • Reperfusion Injury / pathology
  • Reperfusion Injury / physiopathology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors

Substances

  • FR 167653
  • Interleukin-1
  • Pyrazoles
  • Pyridines
  • Tumor Necrosis Factor-alpha