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Antiarrhythmic effect of ischemic preconditioning during low-flow ischemia : The role of bradykinin and sarcolemmal versus mitochondrial ATP-sensitive K+ channels

Driamov, Sergey ; Bellahcene, Mohamed ; Ziegler, André ; Barbosa, Vânia ; Traub, David ; Butz, Silvia ; Buser, Peter ; Zaugg, Christian

In: Basic Research in Cardiology, 2004, vol. 99, no. 4, p. 299-308

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    Titel
    • Antiarrhythmic effect of ischemic preconditioning during low-flow ischemia
      The role of bradykinin and sarcolemmal versus mitochondrial ATP-sensitive K+ channels
    Autor
    • Driamov, Sergey. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    • Bellahcene, Mohamed. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    • Ziegler, André. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    • Barbosa, Vânia. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    • Traub, David. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    • Butz, Silvia. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    • Buser, Peter. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    • Zaugg, Christian. Experimental Cardiology Research Group, Department of Research, University Hospital, Hebelstrasse 20, ZLF 319, 4031, Basel, Switzerland
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • Basic Research in Cardiology, 2004, vol. 99, no. 4, p. 299-308. Steinkopff-Verlag
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:315021
    Summary
    Abstract. : Short episodes of ischemia (ischemic preconditioning) protect the heart against ventricular arrhythmias during zero-flow ischemia and reperfusion. However, in clinics, many episodes of ischemia present a residual flow (low-flow ischemia). Here we examined whether ischemic preconditioning protects against ventricular arrhythmias during and after a low-flow ischemia and, if so, by what mechanism(s). Isolated rat hearts were subjected to 60 min of low-flow ischemia (12% residual coronary flow) followed by 60 min of reperfusion. Ischemic preconditioning was induced by two cycles of 5 min of zero-flow ischemia followed by 5 and 15 min of reperfusion, respectively. Arrhythmias were evaluated as numbers of ventricular premature beats (VPBs) as well as incidences of ventricular tachycardia (VT) and ventricular .brillation (VF) during low-flow ischemia and reperfusion. Ischemic preconditioning significantly reduced the number of VPBs and the incidence of VT and of VF during low-flow ischemia. This antiarrhythmic effect of preconditioning was abolished by HOE 140 (100 nM), a bradykinin B2 receptor blocker. Similar to preconditioning, exogenous bradykinin (10 nM) reduced the number of VPBs and the incidence of VT and of VF during low-flow ischemia. Furthermore, the antiarrhythmic effects of both ischemic preconditioning and bradykinin were abolished by glibenclamide (1 µM), a non-specific blocker of ATP-sensitive K+ (KATP) channels. Finally, the antiarrhythmic effects of both ischemic preconditioning and bradykinin were abolished by HMR 1098 (10 µM), a sarcolemmal KATP channel blocker but not by 5-hydroxydecanoate (100 µM), a mitochondrial KATP channel blocker. In conclusion, ischemic preconditioning protects against ventricular arrhythmias induced by low-flow ischemia, and this protection involves activation of bradykinin B2 receptors and subsequent opening of sarcolemmal but not of mitochondrial KATP channels