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)

Tubular transport abnormalities have recently been characterized in a rabbit model of ischemic acute renal failure (ARF). These studies demonstrated severe observable morphologic and functional changes in the proximal nephron together with functional changes in the distal nephron. Tubular debris was often produced by perfusion of proximal nephron segments. In the present study, agents used to prevent ARF were tested in this rabbit model of ARF. Rabbits were infused with either 5% body wt 5% manitol or 20 micrograms . kg-1 . min-1 furosemide in 5% body wt normal saline for the 60 min preceding 60 min of total renal ischemia. Mannitol 1) prevented the development of ARF, 2) maintained fluid reabsorption in the proximal convoluted tubule (PCT) (0.59 +/- 0.03 vs. 0.52 +/- 0.1 nl . mm-1 . min-1) and proximal straight tubule (PST) (0.34 +/- 0.05 vs. 0.39 +/- 0.07 nl . mm-1 . min-1), 3) depressed NaCl reabsorption in the cortical thick ascending limb of Henle's loop (TALH), and 4) did not prevent a decrease in ADH-mediated osmotic water flow in the cortical collecting tubule (CCT). Furosemide 1) partially preserved renal function, 2) partially protected the PCT (0.63 +/- 0.05 vs. 0.38 +/- 0.04 nl . mm-1 . min-1) and PST (0.32 +/- 0.04 vs. 0.22 +/- 0.02 nl . mm-1 . min-1), and 3) did not change the transport capacity of the TALH or the ADH response of the CCT. Preservation of proximal nephron integrity was also reflected by the absence of debris formation. There is a direct relation between an agent's ability to protect the functional integrity of the cells of the proximal nephron and its ability to preserve renal function.
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PMID:Prior mannitol and furosemide infusion in a model of ischemic acute renal failure. 679 34

Renal artery occlusion has been extensively used in animal models to cause acute renal failure. The present isolated tubule microperfusion studies were designed to examine the transport characteristics of multiple nephron segments of the rabbit after 60 min of total renal ischemia. Preliminary studies showed that this maneuver produced significant and persistent elevations of serum creatinine. The tubules were perfused and bathed with artificial solutions simulating ultrafiltrate and studied at 37 degrees C. Four nephron segments were examined. Ischemia reduced proximal convoluted tubule fluid reabsorption 77% (0.72 +/- 0.11 vs. 0.14 +/- 0.06 nl . mm-1 . min-1, P less than 0.01) and cortical proximal straight tubule fluid reabsorption 88% (0.54 +/- 0.10 vs. 0.06 +/- 0.03 nl . mm-1 . min-1, P less than 0.005). Ischemia reduced the ability of the thick ascending limb of Henle's loop to lower perfusate chloride ion concentration 60% (-47 +/- 9 vs. -19 +/- 3 meq/liter, P less than 0.02) and its diluting ability 49% (-87 +/- 15 vs. -44 +/- 7 mosmol/kg H2O, P less than 0.01). Ischemia reduced the antidiuretic hormone-dependent osmotic water permeability of the cortical collecting tubule 59% (0.0203 +/- vs. 0.0083 +/- 0.0020 cm/s, P less than 0.01). Morphologic alterations were noted in the proximal segments but not in the distal segments of the nephron. The current studies demonstrate that 60 min of renal ischemia impairs the transport capability of all proximal and distal nephron segments studied.
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PMID:Isolated nephron segments in a rabbit model of ischemic acute renal failure. 739 91