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Medizinische Klinik III, Universität zu Köln, D-50924 Cologne, Germany
Received 29 October 1996; accepted in final form 25 March 1997.
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
1- and
2-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+]i
depending 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).
fura 2; heart failure; isoprenaline; ouabain; EMD-57033
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