© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Inotropic response of stunned hypertrophied myocardium: responsiveness of hypertrophied and normal postischemic isolated rat hearts to calcium and dopamine stimulation
Medizinische Universitätsklinik, Abt. III; Eberhard-Karls-Universität Tübingen, Otfried-Müller-Straße 10, D-72076 Tübingen, Germany
* Corresponding author. Tel.: +49 (7071) 29-82088/82712; fax: +49 (7071) 29-2088.
Objective: Severely hypertrophied myocardium was described to have a reduced tolerance towards ischemia. For non-hypertrophied hearts inconclusive findings on the Ca2+-responsiveness are reported. Information on sensitivity to reversible ischemia and on postischemic Ca2+-responsiveness of hearts with clinically common moderate hypertrophy is lacking. Thus, the responsiveness of hypertrophied and normal postischemic myocardium to positive inotropic stimulation should be investigated in the present study. Methods and results: Hearts from spontaneously hypertensive rats (SHR, 4 months old) with significant LV-hypertrophy (+50%) and hearts from normotensive 4 months old Wistar rats were investigated using an isovolumic beating isolated heart model (8 hearts/each of the 8 groups). Functional recovery after 30 min of no-flow ischemia was 78±1% and 77±3% of preischemic control data in hypertrophied and non-hypertrophied hearts assessed as developed left ventricular pressure (non-ischemic controls: 95±2% in hypertrophied and 93±3% in non-hypertrophied controls). Maximum short-term stimulation with Ca2+ revealed a decreased peak left ventricular pressure of 124±4% in hypertrophied and 120±5% in non-hypertrophied postischemic hearts, as compared with non-ischemic controls 138±3% and 157±5%, respectively (p<0.01). A maximum dose of dopamine stimulated hypertrophied and non-hypertrophied postischemic hearts comparable to Ca2+. Analysing the dose–response curve for Ca2+-stimulation, the sensitivity expressed as fraction of the maximum was identical in non-ischemic and postischemic myocardium of hypertrophied and non-hypertrophied ventricles in spite of the reduced peak values. Conclusion: The findings demonstrate that after moderate reversible ischemia the steady-state function is similarly decreased in hypertrophied and non-hypertrophied postischemic myocardium. The maximum response to Ca2+ is significantly reduced in both types of myocardium, while the Ca2+ sensitivity is unchanged. Identical results after maximum dopamine stimulation as after Ca2+ indicate that the releasibility of Ca2+ and the β-adrenoceptors are not the critical causes for the postischemic dysfunction in hypertrophied or non-hypertrophied myocardium.
KEYWORDS Postischemic myocardium; Hypertrophy; Inotropic stimulation; Dopamine
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