Document Detail

Calcium interferes with the cardiodepressive effects of beta-blocker overdose in isolated rat hearts.
MedLine Citation:
PMID:  2872335     Owner:  NLM     Status:  MEDLINE    
Propranolol, timolol and sotalol were compared with respect to their cardiotoxic properties in isolated, spontaneously beating rat hearts. Propranolol and timolol induced a dose-dependent decrease in myocardial contractility. A high dose of sotalol had only modest negative inotropic effects. Similar reductions in myocardial contractility were observed in isolated, ventricle-stimulated rat hearts. These observations were similar to those in a previous study in which spontaneously beating and ventricle-stimulated reserpinized rat hearts were investigated. Spontaneously beating rat hearts were perfused with a high-, a normal- and a low-Ca++ medium, each with and without propranolol, timolol and sotalol. Addition of each beta-blocker to a normal-Ca++ medium induced a decrease of myocardial contractility and of heart rate and an increase of AV-conduction time when compared with the drug-free medium. In a high-Ca++ medium containing the same concentration of each beta-blocker, a less pronounced decrease of myocardial contractility was observed. Heart rate decreased and AV-conduction time increased to the same extent as after perfusion with the drug containing normal-Ca++ medium. With respect to the corresponding drug-free medium perfusion with a low-Ca++ medium with each beta-blocker enhanced the decline in myocardial contractility, most pronounced in propranolol and timolol containing media. For propranolol and sotalol the decrease in heart rate and increase in AV-conduction time were similar to the results after administration of the same beta-blocker in a high- and a normal-Ca++ perfusion media. Timolol caused an electromechanical dissociation. It was concluded that in beta-blocker intoxication the negative-inotropic phenomena cannot be explained by an action of the drugs on the beta-receptor since the results in reserpinized and non-reserpinized rat hearts were similar. Other effects have to be responsible for the observed cardiotoxic phenomena. The present results indicate that these phenomena can be influenced by Ca++ and or can be attributed to differences in lipophilicity.
J Langemeijer; D de Wildt; G de Groot; B Sangster
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Journal of toxicology. Clinical toxicology     Volume:  24     ISSN:  0731-3810     ISO Abbreviation:  J. Toxicol. Clin. Toxicol.     Publication Date:  1986  
Date Detail:
Created Date:  1986-06-27     Completed Date:  1986-06-27     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8213460     Medline TA:  J Toxicol Clin Toxicol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  111-33     Citation Subset:  AIM; IM    
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MeSH Terms
Adrenergic beta-Antagonists / antagonists & inhibitors,  poisoning*
Calcium / pharmacology,  physiology*
Catecholamines / physiology
Coronary Circulation / drug effects
Electric Stimulation
Heart / drug effects*
Heart Conduction System / drug effects
Heart Rate / drug effects
Myocardial Contraction / drug effects
Propranolol / antagonists & inhibitors,  poisoning
Rats, Inbred Strains
Sotalol / antagonists & inhibitors,  poisoning
Timolol / antagonists & inhibitors,  poisoning
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Catecholamines; 26839-75-8/Timolol; 3930-20-9/Sotalol; 525-66-6/Propranolol; 7440-70-2/Calcium

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

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