Document Detail


New inotropic concepts: rationale for and differences between calcium sensitizers and phosphodiesterase inhibitors.
MedLine Citation:
PMID:  9142431     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Positive inotropic compounds may be harmful in the long-term treatment of chronic congestive heart failure because they may induce a calcium overload, unwanted changes in cross-bridge kinetics and an acceleration in heart rate. As a result of all three alterations, energy consumption would be increased. Different pharmacological modes of action may have different effects on the molecular mechanisms underlying the positive inotropic effect, and hence on myocardial energy consumption. Therefore, we studied the effects of a variety of cardiotonic agents on the heat released from small guinea pig papillary muscles contracting isometrically at an experimental temperature of 21 degrees C and a stimulation frequency of 12 per minute using rapid antimony-bismuth thermopiles. We were able to define the economy of muscle contraction, which was lowest with phosphodiesterase inhibitors and highest with calcium sensitizers. Compared with an increase in extracellular calcium concentration, beta 1-adrenoceptor stimulators and phosphodiesterase inhibitors profoundly decrease the economy of myocardial contraction, and calcium-sensitizers (pimobendan and EMD-53998) slightly increase myocardial economy, whereas ouabain and the calcium channel agonist BAY K 8644 have no effect on this parameter. In addition, we provide evidence that acceleration of heart rate may be harmful not only from an energetic point of view: an increase in heart rate may also decrease the contractility of the failing human myocardium (inverse force-frequency relationship). Taking these observations into consideration, an "optimal' positive inotropic compound should have no, or even negative, chronotropic effects, should not be mediated by increases in calcium transients, and should decelerate, rather than accelerate, cross-bridge kinetics.
Authors:
C Holubarsch
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiology     Volume:  88 Suppl 2     ISSN:  0008-6312     ISO Abbreviation:  Cardiology     Publication Date:  1997  
Date Detail:
Created Date:  1997-07-10     Completed Date:  1997-07-10     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  1266406     Medline TA:  Cardiology     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  12-20     Citation Subset:  IM    
Affiliation:
Department of Cardiology and Angiology, University of Freiburg, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / pharmacology*
Cardiotonic Agents / pharmacology*
Deoxyepinephrine / pharmacology
Energy Metabolism
Guinea Pigs
Heart Failure / physiopathology
Humans
Imidazoles / pharmacology
Isoproterenol / pharmacology
Myocardial Contraction / drug effects*
Myocardium / metabolism
Papillary Muscles / drug effects
Phosphodiesterase Inhibitors / pharmacology*
Pyridazines / pharmacology
Pyridones / pharmacology
Quinolines / pharmacology
Thiadiazines / pharmacology
Chemical
Reg. No./Substance:
0/Cardiotonic Agents; 0/Imidazoles; 0/Phosphodiesterase Inhibitors; 0/Pyridazines; 0/Pyridones; 0/Quinolines; 0/Thiadiazines; 119615-63-3/olprinone; 120223-04-3/EMD 53998; 501-15-5/Deoxyepinephrine; 74150-27-9/pimobendan; 7440-70-2/Calcium; 7683-59-2/Isoproterenol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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