December 1, 1988European Journal of Clinical Investigation
Positive inotropic effects in isolated ventricular myocardium from non‐failing and terminally failing human hearts
Population
Isolated, electrically driven papillary muscle strips from terminally failing human hearts or non-failing…
Comparison
Isoprenaline, dobutamine, histamine, forskolin… vs Non-failing donor myocardium and calcium
Design
Preclinical
Authors
Discussion
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Implication
Preserved downstream inotropy in terminal HF cautions against receptor-dependent agents; leaves open Gs modulation as a research target.
Key Points
- To investigate the positive inotropic responses of isolated myocardium from non-failing and terminally failing human hearts.
- Evaluated the inotropic response of isolated papillary muscle strips to various agents including isoprenaline, dobutamine, and calcium.
- Compared maximal contractile response to agents stimulating adenylate cyclase and phosphodiesterase inhibitors in both heart types.
- Analyzed effects relative to muscle strip diameter.
- In non-failing hearts, no significant difference in maximal inotropic effects among isoprenaline, dobutamine, and others, all greater than histamine.
- Terminally failing hearts showed reduced responses to isoprenaline, dobutamine, and IBMX compared to non-failing hearts.
- Forskolin, db-cAMP, and ouabain produced maximal responses similar to calcium in failing hearts.
Structured PICO
P
Population
Isolated, electrically driven papillary muscle strips from terminally failing human hearts or non-failing donor myocardium
I
Intervention
Isoprenaline, dobutamine, histamine, forskolin, isobutyl-methylxanthine (IBMX), dibutyryl-cyclic adenosine monophosphate (db-cAMP), ouabain and calcium
C
Comparator
Non-failing donor myocardium (for failing hearts) and calcium (for maximal force of contraction)
O
Outcome
Positive inotropic effect (force of contraction)surrogate
Terminally failing human hearts show a defect in the regulatory stimulatory subunit (Gs) of adenylate cyclase, reducing the inotropic response to receptor-dependent stimulators.
Cite This Study
Näbauer et al. (1988) studied this question.