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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 24 (1998), S. 743-745 
    ISSN: 1432-1238
    Keywords: Key words Fibrillation ; Defibrillation ; Muscle damage ; Electroporation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 37-year-old Italian male developed a myocardial infarct with subsequent ventricular fibrillation. He was defibrillated seven times with up to 360 Joules. Thirteen days later the patient died of recurrent myocardial infarct due to thrombotic occlusion of the left circumflex coronary artery. At autopsy, necrosis of the right pectoralis muscle was observed. Electroporation is the pathogenetic mechanism of skeletal muscle damage due to multiple defibrillations with high energy levels.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 416 (1990), S. 526-532 
    ISSN: 1432-2013
    Keywords: Aldosterone ; MDCK cells ; Dome formation ; Differentiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vectorial transport of salt and water in the Madin-Darby canine kidney (MDCK) cell line is indicated by the formation of domes when a monolayer is grown on an impermeable support. We investigated aldosterone-induced dome formation and evaluated the dome as an experimental model. Transepithelial dome resistance was about 80 Ωcm2 and constant when dome size exceeded 2 · 10−4 cm2. The relative ion conductances (expressed as transference numbers) across the dome epithelium were t Na∶t Cl∶t K= 0.64∶0.24∶0.06. They reflect the permeability properties of the paracellular shunt pathway tested at physiological concentrations of the individual ions. Aldosterone accelerated dome formation in serum-deprived MDCK monolayers. Prostaglandin E1 and transferrin were supportive but not essential for aldosterone-induced dome formation. After 72 h dome density was equal in monolayers cultured in serum-supplemented medium either in the presence or absence of mineralocorticoids. We conclude that aldosterone induces cell polarization in MDCK monolayers, leading to the formation of domes. The dome epithelium appears to be electrically isolated from the adjacent monolayer and can be studied by microelectrode techniques.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 416 (1990), S. 540-547 
    ISSN: 1432-2013
    Keywords: MDCK cells ; Omeprazole ; H+-K+ pump ; Carbonic anhydrase ; Intercalated cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Functionally and morphologically, Madin-Darby canine kidney (MDCK) cells resemble intercalated cells of urinary epithelia. Experiments were performed on domes of confluent MDCK monolayers to test for apical H+ secretion. Apical application of 10−3 mol/l amiloride or of Na+-free solution significantly reduced the limiting pH gradient across the dome epithelium (Δ pHd) consistent with inhibition of apical Na+/H+ exchange. Short-circuit current (SCC) measurements disclosed an acetazolamide-sensitive, (basolateral to apical) positive transepithelial current stimulated by 10−7 mol/l aldosterone and inhibited by acidification of apical medium to pH=4.5. Histochemical evaluation of carbonic anhydrase (CA) activity revealed cytoplasmic and apicalmembrane-bound CA particularly in dome-forming cells. Apical substitution of Na+ by K+ increased Δ pHd, whereas a reduction of K+ concentration to 0.5 mmol/l or addition of barium or omeprazole (10−5 mol/l) to the apical superfusate reduced Δ pHd by at least 75%. Aldosterone-stimulated SCC was completely abolished by the apical application of barium. We conclude that besides Na+/H+ exchange MDCK cells can express an apically located H+-K+ pump stimulated by aldosterone and inhibited directly by the anti-ulcer agent omeprazole or indirectly, either by blocking apical K+ recycling or by interfering with the CA-dependent intracellular formation of H+ ions.
    Type of Medium: Electronic Resource
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