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  • Title: Energy generation in hypertrophied postischemic myocardium. Feasibility of prolonged inotropic stimulation with dopamine in hypertrophied reperfused left ventricles.
    Author: Hoffmeister HM, Kappelmann A, Beyer ME, Seipel L.
    Journal: Basic Res Cardiol; 1998 Jun; 93(3):201-8. PubMed ID: 9689446.
    Abstract:
    BACKGROUND: Non-hypertrophied reversibly injured postischemic myocardium can be stimulated for a prolonged period without detrimental effects. Since no data on hypertrophied myocardium are available, our aim was to examine the effects of a prolonged postischemic positive inotropic stimulation on moderately hypertrophied left ventricles. METHODS: Using a Langendorff-type isovolumically contracting isolated heart model, moderately hypertrophied (+50% of ventricular mass) hearts from spontaneously hypertensive rats (SHR) were investigated and compared to data from non-hypertrophied hearts of normotensive rats. A 30 minutes noflow ischemia was performed, and in the postischemic period dopamine was continuously administered for 20 minutes in order to stimulate the postischemic hearts to the control level of function. Data were compared to postischemic hearts without stimulation and to non-ischemic controls. After 50 minutes of reperfusion and cessation of the catecholamine steady state function, maximum contractile response, and high energy phosphates were determined. RESULTS: 30 minutes ischemia followed by 50 minutes reperfusion caused a significant reduction in developed LVP to 77.8 +/- 4.2% in SHR. Dp/dtmax was reduced to 67.0 +/- 2.3%. After cessation of dopamine stimulation developed LVP was 64.3 +/- 3.5% and dp/dtmax 69.3 +/- 3.7% in SHR. The double product was identically reduced in all postischemic groups. The contractile reserve was comparable in stimulated and non-stimulated postischemic SHR hearts. In hypertrophied myocardium, ATP was reduced to 1.1 +/- 0.1 mumol/gww (non-ischemic controls 2.5 +/- 0.3 mumol/gww) in unstimulated and to 1.0 +/- 0.1 mumol/gww in stimulated postischemic hearts. Comparably the ischemia-induced reduction in ATP in non-hypertrophied myocardium was 1.3 mumol/gww. Similar results were obtained for ADP and AMP. Creatine phosphate levels were normal in stimulated and non-stimulated postischemic myocardium of hypertrophied and non-hypertrophied hearts. CONCLUSION: These results indicate that prolonged stimulation of stunned hypertrophied myocardium is feasible without detrimental effects on post-stimulation contractile function. The energy generating apparatus is capable to deliver sufficient energy during stimulation of stunned hypertrophied hearts.
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