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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 717 (1994), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 717 (1994), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Medicine 44 (1993), S. 27-37 
    ISSN: 0066-4219
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 18 (1997), S. 0 
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: To investigate the potential direct nephrotoxicity of Shiga toxin, a putative mediator for hemolytic uremic syndrome, purified toxin (10−11 M) was added to isolated rat kidneys perfused for 160 min with a Krebs-Henseleit acellular medium enriched with albumin and amino acids. Kidney function and morphology were examined after perfusion with the Shiga toxin vs controls. Shiga toxin did not significantly alter renal perfusion flow, glomerular filtration rate, or tubular sodium reabsorption, but it significantly increased urinary protein excretion (from 61±23 to 169±28 μg/min, P〈0.01). On renal morphologic study, Shiga toxin did not induce gross glomerular damage but increased markedly the injury to the medullary thick ascending limbs. In conclusion, Shiga toxin is toxic to rat kidneys ex vivo and in the absence of platelets. Renal damage is manifested by proteinuria and medullary tubular injury. The distribution of this injury suggests a possible synergism between local medullary hypoxia and the toxic tubular or endothelial effects of the toxin. These effects may play a pathogenic role in the tubulo-interstitial injury observed in hemolytic uremic syndrome associated with severe renal failure.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 414 (1989), S. 429-437 
    ISSN: 1432-2307
    Keywords: Polyethylene glycol ; Perfused kidney ; Hypoxia ; Proximal tubules ; Distal tubules
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Polyethylene glycol protects against O2 deprivation after clamping of the renal artery or norepinephrine infusion and in hypoxic primary cell culture. Isolated perfused kidneys under hypoxic conditions develop morphological alterations in all segments of the proximal tubule and medullary thick ascending limb. In an attempt to ameliorate the effect of hypoxia, rat kidneys were perfused for 90 min with regularly oxygenated (95% O2+5% CO2) or hypoxic perfusate (95% N2+ CO2) supplemented with 8–12% polyethylene glycol (MW ∼8000). In oxygenated and hypoxic kidneys, polyethylene glycol produced similar changes in S1–S2 segments consisting of reduction of cell thickness and organelle compaction with internalization of brush border into the tubulo-vesicular system. In the S3 segment, the cellular volume loss was more limited; the brush border was transformed to membranous whorls and the cytoplasm contained large, irregular, clear zones. Mitochondrial swelling was pronounced in the hypoxic proximal tubules. Polyethylene glycol quantitatively increased and emphasized the damage in the medullary thick ascending limb. Inclusion of 10−2 M ouabain preserved the medullary thick ascending limb from hypoxic injury and polyethylene glycol had no effect on this undamaged epithelium. Thus, polyethylene glycol affects renal tubules on the basis of their known water permeability and does not protect against but rather worsens hypoxic injury in the medullary thick ascending limb.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 42 (1986), S. 570-572 
    ISSN: 1420-9071
    Keywords: Anoxic injury ; mitochondrial respiration ; renal medulla ; acute renal failure ; renal metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary In brain1, heart2 and kidney3, cell work in the absence of oxygen has been thought to precipitate anoxic damage by increasing the rate of depletion of cellular energy stores. In the medullary thick ascending limb of isolated perfused rat kidneys, however, reduction of ATP synthesis by a variety of mitochondrial or metabolic inhibitors caused ATP depletion comparable to that produced by oxygen deprivation but did not reproduce the lesions of anoxia. In these cells, unrestrained mitochondrial activity may be an important source of anoxic injury.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Journal of Electron Microscopy Technique 9 (1988), S. 293-298 
    ISSN: 0741-0581
    Keywords: Renal medulla ; Isolated perfusion ; Anoxic damage ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Natural Sciences in General
    Notes: The tubular epithelial cells located in the renal medulla are normally working in a hypoxic milieu. In isolated rat kidneys perfused with a cell-free medium, the medullary thick ascending limbs of Henle's loop are selectively and reproducibly injured by the imbalance between oxygen demand and supply in this area. Hypoxic lesions rapidly progress from reversible to irreversible forms of cell damage. Reversible injury consists of chromatin margination and mitochondrial swelling, which can disappear upon restoration of an adequate balance of oxygenation. Irreversible injury consists of nuclear pyknosis and cytoplasmic fragmentation, lesions which persist after re-oxygenation or even progress to cell death. Reversible and irreversible phases of hypoxic injury in this distal tubule segment are comparable to, but different from, those previously defined for the proximal tubule.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
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