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Soluble substances released from postischemic reperfused rat hearts reduce calcium transient and contractility by blocking the L-type calcium channel

Stephan B. Felix, MD^*, Verena Stangl, MD, Peter Pietsch, PhD, Peter Bramlage, MD, Alexander Staudt, MD^*, Sabine Bartel, PhD, Ernst-Georg Krause, MD, J.örn-Uwe Borschke, MD, Klaus-Dieter Wernecke, PhD^||, Gerrit Isenberg, MD and Gert Baumann, MD

^* Klinik für Innere Medizin B, Ernst-Moritz-Arndt-Universität Greifswald, Greifswald, Germany
Medizinische Klinik und Poliklinik Charité, Kardiologie, Campus Mitte, Humboldt-Universität zu Berlin, Berlin, Germany
Max Delbrück Zentrum für molekulare Medizin, Berlin-Buch, Germany
Institut für Physiologie, Universität Halle, Halle, Germany
^|| Institut für Medizinische Biometrie, Charité, Humboldt-Universtät zu Berlin, Berlin, Germany

View larger version (15K): [in a new window]   Figure 1 Fast time-base recording of changes in Fluo-3 fluorescence, expressed as relative fluorescence units (rfu) and cell length (µm) of a single field-stimulated rat cardiomyocyte under basal conditions (control), during superfusion with postischemic coronary effluent (dilution 1:4) and during superfusion with fresh experimental buffer (washout). Effluent = postischemic coronary effluent.

View larger version (25K): [in a new window]   Figure 2 Effects of pooled postischemic coronary effluent at different dilutions on systolic cell shortening, Ca2+ transient (peak systolic rfu – diastolic rfu) and peak systolic Fluo-3 fluorescence of isolated field-stimulated rat cardiomyocytes. The effects were calculated as percent changes compared with the values under basal conditions (control). The data are presented as the mean value ± SEM for six different myocytes incubated with the indicated dilutions of postischemic effluent. Each cardiomyocyte was used for only a single study employing one of five different dilutions.

View larger version (17K): [in a new window]   Figure 3 Reduction of whole-cell ICa by the postischemic coronary effluent. A, ICa recorded from a rat ventricular myocyte before (control; solid circles) and 1 min after adding 1:4 diluted postischemic effluent to the superfusate (open circles). The time-dependent decay of ICa was matched to a double-exponential function (thin solid line; time constants = 4 and 20 ms). B, Plot of peak ICa as a function of the test-step potential (iv curve) before (control; filled circles) and after adding 1:4 diluted postischemic effluent to the superfusate (open circles). The holding potential was –45 mV. Between –40 and 50 mV, voltage dependence of peak ICa is matched, as calculated from the Boltzman formula. Effluent = postischemic coronary effluent (dilution 1:4).

View larger version (18K): [in a new window]   Figure 4 Time course of the changes in peak ICa (filled circles), the holding current at –50 mV (open squares) and the late current (current measured at the end of the 100-ms pulse to 0 mV; filled triangles) during superfusion with postischemic coronary effluent (dilution 1:4) and during washout.