Transport-dependent anoxic cell injury in the isolated perfused rat kidney.
The hypothesis that decrease in energy demand may prevent anoxic cell damage has been examined in the medullary thick ascending limb of isolated perfused rat kidneys exposed to oxygen deprivation. The effects of decreasing active reabsorptive transport in the medullary thick ascending limb were observed on the extensive damage regularly induced by hypoxic perfusion (gassed with no oxygen) or potassium cyanide. Anoxic injury was consistently attenuated or abolished if reabsorptive transport was decreased with ouabain or furosemide or by halting the glomerular filtration rate with the use of a hyperoncotic medium (nonfiltering kidney). Comparison of the injury generated by warm ischemia for identical time periods showed that complete ischemia does not reproduce the severe lesions seen during hypoxic perfusion. These results suggest that transport activity is a determining factor of anoxic cell death in the thick ascending limb of Henle's loop.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D003470:Culture Media; D005665:Furosemide / Q000494:pharmacology; D007511:Ischemia / Q000473:pathology; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D008138:Loop of Henle / Q000378:metabolism / Q000473:pathology; D008297:Male; D008854:Microscopy, Electron; D010042:Ouabain / Q000494:pharmacology; D010100:Oxygen / Q000502:physiology*; D010477:Perfusion; D011190:Potassium Cyanide / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013696:Temperature
D003470:Culture Media; D010042:Ouabain; D005665:Furosemide; D011190:Potassium Cyanide; D010100:Oxygen