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Vol. 280, Issue 1, 247-254, 1997
From the Integrated Physiology Laboratories, The present study was aimed at investigating the effect of two
Ca++ sensitizers, EMD 57033 (without significant
phosphodiesterase inhibition) and ORG 30029 (with phosphodiesterase
inhibition), in myocardium from nonfailing and failing human hearts. In
nonfailing myocardium both EMD 57033 and ORG 30029 increased force of
contraction by 280 ± 27% and 94 ± 13%, respectively
(n = 6); the time to 80% relaxation
(t80%) by 278 ± 45% and 155 ± 21%; and diastolic force by 28 ± 8% and 12 ± 3%,
respectively. In trabeculae from failing myocardium, the increase in
active force was similar to that in nonfailing trabeculae (EMD,
305 ± 30%; ORG, 88 ± 12% (n = 6)).
However, the increase in t80% (EMD,
378 ± 56%; ORG, 230 ± 26%) and diastolic force (65 ± 12%; 24 ± 5%) was more pronounced in failing myocardium. EMD
had no effect on the peak of the [Ca++]i
transient; however, it prolonged the time course of the
[Ca++]i transient in both nonfailing and
failing myocardial fibers. ORG increased the peak of the
Ca++ transient and prolonged the time course in
preparations from both nonfailing and failing hearts. Both EMD and ORG
shifted the [Ca++]-force relationship toward lower
[Ca++] (EMD > ORG).The Ca++ sensitizers
EMD 57033 and ORG 30029 increased active force development in
nonfailing and failing human myocardium, but both impaired relaxation
in failing myocardium to a greater extent than in nonfailing human
myocardium in a concentration-dependent fashion.
Copyright © by The American Society for Pharmacology and Experimental Therapeutics
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