Further studies of renal preservation: protection of the ischemic kidney with inosine.
Preliminary data are presented on additional means of renal preservation, particularly in the case of warm ischemic insult. We hypothesize that 1 factor responsible for the failure of kidneys to recover after ischemic insult may be depletion of energy sources during the warm ischemic period. Specifically, adenosine triphosphate in the kidney is the principal source of energy for metabolic activity and membrane stability. Inosine, an adenosine triphosphate precursor, was used in a canine model and preliminary work suggested that inosine, when coupled with mannitol, may provide enhanced protection. In vivo assay of kidney slices suggests that inosine may, indeed, tend to maintain adenosine triphosphate levels in the ischemic kidney in contrast to relative adenosine triphosphate depletion in the kidneys not protected with inosine. These data are in concert with the apparently favorable survival data in inosine and mannitol-treated animals.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D004285:Dogs; D007036:Hypothermia, Induced; D007288:Inosine / Q000378:metabolism* / Q000494:pharmacology; D007511:Ischemia / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply / Q000378:metabolism; D016030:Kidney Transplantation; D008353:Mannitol / Q000494:pharmacology; D009926:Organ Preservation / Q000379:methods*; D010477:Perfusion; D051381:Rats; D014021:Tissue Preservation / Q000379:methods*; D014184:Transplantation, Homologous
D008353:Mannitol; D007288:Inosine; D000255:Adenosine Triphosphate