INOTROPIC RESPONSE OF STUNNED HYPERTROPHIED MYOCARDIUM - RESPONSIVENESS OF HYPERTROPHIED AND NORMAL POSTISCHEMIC ISOLATED RAT HEARTS TO CALCIUM AND DOPAMINE STIMULATION

Objective: Severely hypertrophied myocardium was described to have a r educed tolerance towards ischemia. For non-hypertrophied hearts inconc lusive findings on the Ca2+-responsiveness are reported. Information o n sensitivity to reversible ischemia and on postischemic Ca2+-responsi veness of hearts with clinically common moderate hypertrophy is lackin g. Thus, the responsiveness of hypertrophied and normal postischemic m yocardium to positive inotropic stimulation should be investigated in the present study. Methods and results: Hearts from spontaneously hype rtensive rats (SHR, 4 months old) with significant LV-hypertrophy (+ 5 0%) and hearts from normotensive 4 months old Wistar rats were investi gated 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 hypertroph ied and non-hypertrophied hearts assessed as developed left ventricula r pressure (non-ischemic controls: 95 +/- 2% in hypertrophied and 93 /- 3% in non-hypertrophied controls). Maximum short-term stimulation w ith 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 hy pertrophied and non-hypertrophied postischemic hearts comparable to Ca 2+. Analysing the dose-response curve for Ca2+-stimulation, the sensit ivity expressed as fraction of the maximum was identical in non-ischem ic and postischemic myocardium of hypertrophied and non-hyper trophied ventricles in spite of the reduced peak values. Conclusion: The findi ngs demonstrate that after moderate reversible ischemia the steady-sta te function is similarly decreased in hypertrophied and non-hypertroph ied postischemic myocardium. The maximum response to Ca2+ is significa ntly reduced in both types of myocardium, while the Ca2+ sensitivity i s unchanged. Identical results after maximum dopamine stimulation as a fter Ca2+ indicate that the releasibility of Ca2+ and the beta-adrenoc eptors are not the critical causes for the postischemic dysfunction in hypertrophied or non-hypertrophied myocardium. (C) 1998 Elsevier Scie nce B.V.