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European Heart Journal 1991 12(Supplement F):153-156; doi:10.1093/eurheartj/12.suppl_F.153
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Influence of ischaemic cardioplegic arrest on the haemodynamic efficacy of the PDE-III inhibitor, enoximone

J. G. Preuner*,, R. Gieseke, W. Kasper and D. Birnbaum*

Dept. of Cardiovascular Surgery Rehabilitationszentrum, Suedring 15, D-7812 BAD Krozingen, Germany
* Dept. of Cardiovascular Surgery, Universitaetsstr., University of Regensburg D-8400 Regensburg, Germany

Correspondence: J. G. Preuner, Dept. of Cardiovascular Surgery, Universitaetsstr., University of Regensburg, D-8400 Regensburg, Germany

The haemodynamic support from an enoximone infusion (2 x bolus 0·5mg. kg–1, infusion 0·5 µg. kg–1min–1) in the early postischaemic phase is modified by a transient diminution of the drug's positive inotropic and vasodilatory effect (1 to 4h). Forty-five min after weaning off cardiopulmonary bypass (CPB) the initial increase in cardiac index (CI) induced by enoximone (+26±8%) faded and was no longer discernible in the control group. A significant increase in CI was observed again 4–6h after cardioplegic arrest (ultimate steady state values >10h; CI +0·71. min–1 x m–2; +21%). This pharmacodynamic fading occurred in the presence of constant plasma concentrations of enoximone (442±31ng. ml–1) and elevated high plasma norepinephrine (926 ± 70pg. ml–). Two independent processes might be responsible for the ischaemia-induced complex time dependency of the pharmacodynamic effect: (1) sensitization of the adrenergic receptor pathway and/or activation of sarcolemmal Ca-influx, rapidly reversed during reperfusion, and (2) impaired sarcoplasmic reticulum responses, which are slowly repaired after weaning off CPB.

Key Words: Ischaemia • endogenous catecholamines • adrenergic signal transduction pathway • enoximone • PDE-III • cardiac surgery


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