Effect of inotropic interventions on contraction and Ca2+transients in the human heart

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Abstract
Brixius, Klara, Marcus Pietsch, Susanne Hoischen, Jochen Müller-Ehmsen, and Robert H. G. Schwinger. Effect of inotropic interventions on contraction and on Ca2+transients in the human heart. J. Appl. Physiol. 83(2): 652–660, 1997.—The present study investigated the influences of inotropic intervention on the intracellular Ca2+transient {intracellular Ca2+concentration ([Ca2+]i)} and contractile twitch. Isometric twitch and [Ca2+]i(fura 2 ratio method) were measured simultaneously (1 Hz, 37°C) after stimulation with Ca2+(0.9–3.2 mM), the cardiac glycoside ouabain (Oua; 0.1 μM), the β1- and β2-adrenoceptor-agonist isoprenaline (Iso; 1–10 nM), and the Ca2+sensitizer EMD-57033 (30 μM) by using isolated human nonfailing right auricular trabeculae ( n = 19). Inotropic interventions increased force of contraction and peak rate of tension rise (+ T) significantly. Only Iso stimulated peak rate of tension decay (− T) higher than + T ( P< 0.05), thereby reducing time of contraction ( Ttwitch). EMD-57033 increased + T more effectively than − T and prolonged Ttwitch( P < 0.05). Ca2+, Oua, and Iso, but not EMD-57033, increased systolic Ca2+. Diastolic Ca2+increased after stimulation with Oua or Ca2+, but not in the presence of EMD-57033. Iso shortened the Ca2+transient and did not influence diastolic Ca2+. In conclusion, positive inotropic agents differently affect force and [Ca2+]idepending on their mode of action. Inotropic interventions influence diastolic Ca2+and thus may be less advantageous in a situation with altered intracellular Ca2+homeostasis (e.g., heart failure due to dilated cardiomyopathy).