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  • 1
    ISSN: 0014-5793
    Keywords: Anoxia ; Heart cell ; K"A"T"P channel ; Patch clamp
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 51 (1973), S. 754-758 
    ISSN: 1432-1440
    Keywords: Acetylsalicylic acid ; auto-antibodies ; purpura ; thrombocytopenia ; drug-induced cytopenia ; Acetylsalicylsäure ; Autoantikörper ; Purpura ; Thrombocytopenie ; arzneimittelallergische Cytopenie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird über den Fall einer letalen arzneimittelallergischen Thrombocytopenie nach Thomapyrin® berichtet, bei der sich hochtitrige thrombocytäre Antikörper in vitro nachweisen ließen. Die komplementbindenden Antikörper waren spezifisch gegen die Acetylsalicylsäurekomponente im Thomapyrin® gerichtet und inaktiv gegenüber dessen Phenacetinkomponente. Aus dem klinischen Bild ergaben sich Hinweise für kreuzreagierende allergische Reaktionen mehrerer Zellsysteme, besonders auch der hämopoetischen Vorstufen. Der deletäre Verlauf der Cytopenie wird aus der fortgesetzten Einnahme des Medikaments erklärt. Die Seltenheit dieser durch Aspirin® bedingten Thrombocytopenie — bisher wurden erst von einem Autor Antikörper immunologisch nachgewiesen — erschwert die Diagnose des lebensbedrohlichen Krankheitsbildes.
    Notes: Summary This case report deals with drug-induced allergic thrombocytopenia with lethal issue resulting from Thomapyrin®. It was possible to demonstrate the in vitro existence of a high antibody titer against platelets. The complement-binding antibodies were directed specifically against the acetylsalicylic acid, a component of Thomapyrin®, but did not react against its phenacetin component. The clinical picture pointed to cross-reactive allergic reactions of various cell systems, in particular of the hemopoietic precursor cells. The destructive course of the cytopenia can be explained by the continuous intake of the drug. The rare occurrence of this thrombocytopenia caused by Aspirin®—until now, antibodies have been immunologically proven by only one author—renders the diagnosis of this life-threatening disease quite difficult.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 427 (1994), S. 547-549 
    ISSN: 1432-2013
    Keywords: Mouse heart cells ; Transient K+ outward current ; Anoxia ; Down-regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Transient K+ outward currents (I to) were measured in enzymatically isolated ventricular mouse heart cells with a patch clamp technique in the whole cell configuration. Exposure of the cells to substrate-free anoxia gradually decreased both the peak and the late I to. The inactivation time course of I to was fitted with two exponentials. After 4–10 min of anoxia, the contribution of the fast and slow exponential decreased to 60±7% and 62±4% of the control value and recovered after reoxygenation within 1–3 min to 84±5% and 75±6% (n=10; all mean ±SEM), respectively. The time constants of the exponentials were invariant to anoxia. Voltage dependence of activation and inactivation of I to were not influenced by anoxia. Application of stimulators of protein kinase A and C, cGMP-dependent protein kinase, or of the oxidant diamide during anoxia did not recover I to. It is concluded that under conditions of metabolic stress, I to is reversibly down-regulated leaving inactivation kinetics unchanged. The underlying mechanism is as yet unknown but does neither involve a decreased activity of protein kinase A, protein kinase C, nor c-GMP dependent protein kinase.
    Type of Medium: Electronic Resource
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