Free radical ablation for the prevention of post-ischemic renal failure following renal transplantation.
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.
Schiller
H J
HJ
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore.
Andreoni
K A
KA
Bulkley
G B
GB
D058186:Acute Kidney Injury / Q000503:physiopathology*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage; D005609:Free Radicals; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply*; D016030:Kidney Transplantation / Q000502:physiology*; D015227:Lipid Peroxidation / Q000502:physiology*; D009504:Neutrophils / Q000502:physiology; D010100:Oxygen / Q000502:physiology*; D015427:Reperfusion Injury / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000008:administration & dosage
D000975:Antioxidants; D005609:Free Radicals; D013482:Superoxide Dismutase; D010100:Oxygen