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Free radical ablation for the prevention of post-ischemic renal failure following renal transplantation

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Summary

The toxic metabolites of oxygen, including those which are free radicals, have been found to constitute a fundamental common pathway of tissue injury in a wide variety of disease processes, including injury in many organs resulting from post-ischemic reperfusion. Research efforts designed to prevent or ameliorate tissue injury have therefore centered on the pharmacologic inhibition of free radical-mediated mechanisms. This approach has particular application to post-ischemic renal failure seen in renal transplantation, after a well-defined period of graft ischemia, followed by reperfusion.

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Abbreviations

ADCC:

antibody dependent cellular cytotoxicity

DMSO:

dimethyl sulfoxide

DMTU:

dimethylthiourea

EDRF:

endothelium-derived relaxing factor

EDTA:

ethylenediaminetetraacetic acid

GMP 140:

granule membrane protein 140

NO:

nitric oxide

O2 − :

superoxide radical

SOD:

superoxide dismutase

TNF:

tumor necrosis factor

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Authors and Affiliations

  1. Department of Surgery, The Johns Hopkins Medical Institutions, Baltimore

    H. J. Schiller, K. A. Andreoni & G. B. Bulkley

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  1. H. J. Schiller
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  2. K. A. Andreoni
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  3. G. B. Bulkley
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Manuscripts published in this issue were the matter of a Symposium held at the University of Ulm, April 24–27, 1991.

Supported by NIH Grant # DK31764.

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Schiller, H.J., Andreoni, K.A. & Bulkley, G.B. Free radical ablation for the prevention of post-ischemic renal failure following renal transplantation. Klin Wochenschr 69, 1083–1094 (1991). https://doi.org/10.1007/BF01645163

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