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Related Experiment Videos

Oxygen free radical mediated renal dysfunction.

J A Galat1, A V Robinson, R S Rhodes

  • 1Department of Surgery, Case Western Reserve University, Cleveland, Ohio 44106.

The Journal of Surgical Research
|May 1, 1989
PubMed
Summary
This summary is machine-generated.

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Oxygen free radicals (OFRs) significantly reduce kidney function, decreasing glomerular filtration more than renal blood flow. OFRs contribute to postischemic renal dysfunction, but ischemia likely causes tubular damage.

Area of Science:

  • Nephrology
  • Physiology
  • Biochemistry

Background:

  • Postischemic renal dysfunction (PIRD) involves reduced glomerular filtration and tubular reabsorption.
  • The role of oxygen free radicals (OFRs) in PIRD is not fully understood.

Purpose of the Study:

  • To investigate the direct renal effects of OFRs, independent of ischemic injury.
  • To determine the contribution of OFRs to the hemodynamic and filtration changes seen in PIRD.

Main Methods:

  • Isolated rat kidneys were perfused with a Krebs' buffer.
  • Oxygen free radicals were generated by infusing hypoxanthine and xanthine oxidase.
  • Effects on vascular resistance, flow rate, glomerular filtration rate, and tubular function were measured.

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Main Results:

  • OFR generation increased vascular resistance by 50%, reduced perfusate flow by 30%, and decreased glomerular filtration rate by 70%.
  • Urine flow and oxygen consumption also decreased significantly.
  • Tubular reabsorption of water and sodium remained unaffected.
  • These effects were abolished by inactivating xanthine oxidase or using antioxidants (superoxide dismutase and catalase).

Conclusions:

  • OFRs independently cause a disproportionate decrease in glomerular filtration compared to renal blood flow, mimicking PIRD.
  • OFRs likely contribute to the hemodynamic and glomerular alterations observed in PIRD.
  • Ischemia, rather than OFRs, is likely responsible for the observed tubular dysfunction.