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Cardiovascular Research 1997 35(1):68-79; doi:10.1016/S0008-6363(97)00105-3
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Release of a stable cardiodepressant mediator after myocardial ischaemia during reperfusion1

Stephan B Felix*, Verena Stangl, Thomas M Frank, Claudia Harms, Thomas Berndt, Reinhard Kästner and Gert Baumann

Medizinische Klinik und Poliklinik I, Charité, Humboldt-Universität zu Berlin, Schumannstr. 20–21, D-10098 Berlin, Germany

* Corresponding author. Tel.: +49 (30) 2802-5885; fax.: +49 (30) 2802-3996.

Objective: The aim of this study was to investigate whether cardiodepressant mediators are released after myocardial ischaemia during reperfusion. Methods: Using a double heart model, the effect of the reoxygenated coronary effluent of an isolated guinea pig heart on a sequentially perfused second heart was studied under control conditions and after 10 min ischaemia of the first heart. Investigation of the modulating role of known autacoids took place by using free radical scavengers, an NO synthase inhibitor and adenosine receptor antagonists. In order to identify the chemical nature of cardiac metabolites, the coronary effluent was also subjected to different chemical treatment modes. Results: No haemodynamic changes were observed during sequential perfusion under control conditions. After 10 min of global ischaemia in heart I, a marked decrease in LVP (–22%), LVdP/dtmax (–43%), LVdP/dtmin (–41%) and coronary perfusion pressure (–25%) was measured in heart II during sequential perfusion. The negative inotropic effect was rapid in onset and reversible within 5 min; free radicals, nitric oxide and adenosine were not involved. Storage of the coronary effluent of the first heart up to 24 h, heating, or protease treatment did not modify its cardiodepressant effects on the second sequentially perfused heart. Conclusions: These results suggest the release—from an isolated heart after ischaemia during reperfusion—of a cardiodepressant mediator which induces a potent reversible negative inotropic effect on a sequentially perfused heart. The mediator is stable and in all probability not a protein.

KEYWORDS Myocardial ischemia; Reperfusion; Cardiodepression; Free radicals; Free radical scavengers; Guinea pig, heart

1 Part of this work was presented at the Joint meeting of the European Society of Cardiology, in Birmingham, on August 25–29, 1996.


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