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Effects of cantharidin on force of contraction and phosphatase activity in nonfailing and failing human hearts
Author(s) -
Linck Bettina,
Boknik Peter,
Knapp Jörg,
Müller Frank U.,
Neumann Joachim,
Schmitz Wilhelm,
Vahlensieck Ute
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15706.x
Subject(s) - cantharidin , inotrope , medicine , contraction (grammar) , endocrinology , cardiology , chemistry , organic chemistry
1 The effect of the phosphatase inhibitor, cantharidin (3–300 μ m ) on force of contraction was studied in isolated electrically driven right ventricular trabeculae carneae from human myocardium. 2 The positive inotropic effect of cantharidin started at a concentration of 100 μ m with a positive inotropic effect to 199% and to 276% of the predrug value in nonfailing and failing human hearts, respectively. 3 Under basal conditions the contraction time parameters were prolonged in human heart failure vs. nonfailing preparations. However, the positive inotropic effect of cantharidin did not affect contraction time parameters. Thus, time to peak tension, time of relaxation and total contraction time were not shortened by cantharidin in nonfailing and failing preparations. 4 The phosphatase activity was unchanged in preparations from failing hearts compared to nonfailing hearts. 5 Cantharidin inhibited phosphatase activity in a concentration‐dependent manner. The IC 50 value of cantharidin was about 3 μ m in both nonfailing and failing human myocardium. 6 The positive inotropic effect of cantharidin was similar in nonfailing and failing human hearts, accompanied by a similar inhibitory effect of cantharidin on the phosphatase activity. The positive inotropic effect of cantharidin in failing hearts was as strong as the effect of isoprenaline in nonfailing hearts. 7 It is concluded that the treatment with a phosphatase inhibitor may offer a new positive inotropic modality for the treatment of human heart failure.