Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this investigation was to test the effects of glycine, a cytoprotectant in normothermic in vitro models of renal ischemia, in a model of hypothermic renal preservation injury. This study also probes possible physiological mechanisms of glycine protection during renal hypothermic ischemia-reperfusion injury. Canine kidneys were subjected to 48 h of hypothermic ischemia (4 degrees C) after intravascular flush with cold conventional Collins solution (G. H. Collins, M. B. Bravo-Shugarman, and P. I. Terasaki, Lancet 2: 1219-1223, 1969) and were subsequently revascularized for 1 h. After 1 h of reperfusion, glomerular filtration rate, urine production, and electrolyte excretion were dramatically higher when the Collins flush contained 5 mM glycine, compared with the 0 mM glycine controls. Renal tissue adenine nucleotides and glutathione levels progressively declined with graded cold ischemia times, and glycine had no effect on these levels. However, renal tissue ATP levels (but not glutathione) were significantly higher when kidneys were flushed with glycine, stored for 48 h, and reoxygenated in vitro for 1 h at 37 degrees C, compared with kidneys flushed without glycine. Analysis of CoA esters from ischemic renal tissue indicated altered production of only butyryl CoA after 48 and 72 h of cold ischemia, but no differences were detected in glycine or control kidneys. In conclusion, this study reports dramatic functional preservation with glycine in kidneys subjected to hypothermic ischemia and in vivo reperfusion. The mechanisms of these effects appear not to be attributable to the maintenance of cellular adenine nucleotide or glutathione levels nor to the scavenging of accumulated amphipathic acyl CoA esters.
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PMID:Protective effects of glycine during hypothermic renal ischemia-reperfusion injury. 195 15

The effects of hypothermic ischemia utilizing Euro-Collins flush on renal tissue long-chain activated fatty acid content was studied in dogs. Also, the ability of the simple amino acid glycine to complex these acyl thioesters was also investigated. Renal inner cortex was found to contain (in increasing amounts) myristoyl-, palmitoleoyl-, palmitoyl-, arachidonyl-, and oleoyl-coenzyme A throughout the 3 days of cold ischemia. Although the amounts of individual long-chain acyl-CoA compounds varied considerably, the concentrations were not found to differ significantly with increasing ischemia times. The presence of 5 mM of glycine in the flush also did not influence the amount or species of long-chain acyl-CoA esters in renal tissue during cold ischemia. Ischemic renal tissue content of most long-chain acyl-CoA compounds was reduced by about 50% when the tissue underwent in vitro reperfusion with 37 degrees C O2-saturated media. Glycine included in the flush storage solution did not alter acyl-CoA levels in tissue undergoing hypothermic ischemia and short-term in vitro reperfusion with O2-saturated buffer. In conclusion, long-chain acyl-CoA thioesters are present during hypothermic renal ischemia and the levels of most of these species are reduced during in vitro reperfusion after ischemia. The quality and production mass of these metabolites appears to be unaltered by progressive hypothermic ischemia times. Finally, the protective effects of glycine in this model of renal organ preservation injury are not associated with reductions of renal tissue long-chain activated fatty acids.
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PMID:Long-chain acyl-coenzyme A thioesters and renal hypothermic ischemic injury: effects of glycine flush. 844 Jan 27