Alterations in the dog renal tubular epithelium during normothermic ischemia.
Dog kidneys were subjected to one, two, or three hours' normothermic ischemia in situ and were then excised for biochemical and histological evaluation. The uptake of para-aminohippurate (PAH) by cortical slices progressively decreased with prolongation of the ischemia, but active transport was never abolished. Glycine uptake and oxygen consumption were only reduced to a modest extent by the ischemia. The intracellular ion levels were drastically altered, with loss of potassium and gain of sodium and chloride, and considerable increases in tissue water were observed. Acid phosphatase was liberated by the whole organ into the venous blood and by the incubated slices into the incubation medium, but both biochemical and histochemical techniques showed that the total quantity of the enzyme in the cells was hardly changed. The histochemical reaction product was localized exclusively in the lysosomes. Morphological damage was slight after one or two hours' ischemia, but more pronounced after three hours, when some cells were seen to be detached from the basement membrane. These relatively minor changes seem insufficient to predict the ultimate fate of the organ after ischemia.
D000135:Acid Phosphatase / Q000097:blood; D000818:Animals; D004285:Dogs; D004848:Epithelium / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism* / Q000473:pathology; D007668:Kidney / Q000098:blood supply* / Q000473:pathology; D007684:Kidney Tubules / Q000378:metabolism*; D008247:Lysosomes / Q000201:enzymology; D010101:Oxygen Consumption; D013997:Time Factors; D010130:p-Aminohippuric Acid / Q000378:metabolism
D000135:Acid Phosphatase; D005998:Glycine; D010130:p-Aminohippuric Acid