Document Detail

Apparent superiority of H2-receptor stimulation and simultaneous beta-blockade over conventional treatment with beta-sympathomimetic drugs in post-acute myocardial infarction: cardiac effects of impromidine--a new specific H2-receptor agonist-in the surviving catecholamine-insensitive myocardium.
MedLine Citation:
PMID:  6151806     Owner:  NLM     Status:  MEDLINE    
Left ventricular infarction (AMI) was produced in experimental animals and the contractile response to beta-adrenergic and H2-histaminergic stimulation by isoproterenol and impromidine tested in the isolated perfused heart preparation. Adenylate cyclase activity as well as binding characteristics of [3H]-dihydroalprenolol ([3H]-DHA), [3H]-methyl-tiotidine ([3H]-TIOT) and [3H]-quinuclidinyl benzilate ([3H]-QNB) to cardiac beta 1-, H2- and cholinergic muscarinic receptors were determined in sarcolemmal membrane preparations of the right ventricle of the same hearts. In addition, an attempt was made to elucidate the therapeutic value of post-AMI treatment with impromidine in the presence and absence of beta-blockade, in contrast to administration of prenalterol and the conventional therapy with beta-sympathomimetic drugs, e.g. dobutamine. Three days post-AMI the dose-response curve for isoproterenol of right ventricular dP/dtmax was significantly depressed, while the inotropic effect of impromidine was not impaired. Stimulation of adenylate cyclase activity by isoproterenol was reduced by 80% whereas impromidine and NaF stimulation rates were unaltered. Receptor-binding studies indicated a 90% loss and 10-times lowered affinity (KD) of the remaining beta-receptors while specific [3H]-TIOT- and [3H]-QNB-binding was unchanged. Administration of dobutamine increased mortality rates and extension of infarct size, led to a further decrease in contractile response to isoproterenol, induced complete insensitivity of adenylate cyclase to isoproterenol stimulation and caused pronounced additional reduction of number and affinity of [3H]-DHA-binding sites. In contrast, all above alterations were prevented by treatment with either prenalterol or combined administration of impromidine plus metoprolol. It is concluded, that these alterations in the non-ischemic, uninvolved myocardium post-AMI are the result of catecholamine-induced specific damage of sarcolemmal beta-receptors. Furthermore, treatment with H2-agonists in combination with beta-blocking agents may have beneficial effects, whereas conventional therapy with beta-sympathomimetic drugs tends to worsen the already depressed function of the beta-adrenergic stimulation mechanism.
G Baumann; S B Felix; C D Heidecke; G Riess; U Loher; L Ludwig; H Blömer
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Agents and actions     Volume:  15     ISSN:  0065-4299     ISO Abbreviation:  Agents Actions     Publication Date:  1984 Oct 
Date Detail:
Created Date:  1985-03-05     Completed Date:  1985-03-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0213341     Medline TA:  Agents Actions     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  216-28     Citation Subset:  IM    
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MeSH Terms
Adenylate Cyclase / metabolism
Adrenergic beta-Antagonists / therapeutic use*
Binding Sites
Dobutamine / therapeutic use
Guinea Pigs
Imidazoles / therapeutic use*
Myocardial Contraction / drug effects
Myocardial Infarction / drug therapy*,  enzymology,  metabolism,  physiopathology
Myocardium / enzymology,  metabolism
Practolol / analogs & derivatives,  pharmacology
Receptors, Histamine / drug effects*
Receptors, Histamine H2 / drug effects*
Subcellular Fractions / metabolism
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Imidazoles; 0/Receptors, Histamine; 0/Receptors, Histamine H2; 34368-04-2/Dobutamine; 55273-05-7/Impromidine; 57526-81-5/Prenalterol; 6673-35-4/Practolol; EC Cyclase

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

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