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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 626-630 
    ISSN: 1432-1912
    Keywords: Key words Histamine ; Myocardium ; Mast cells ; Autonomic nerve terminals ; Compound 48/80
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Inotropic effects of histamine were examined in isolated ventricular preparations from late embryonic and hatched chick hearts. In 19 day-old embryonic preparations, histamine had little effect on the contractile force. In preparations from 1 to 2 day-old hatched chick, histamine produced a transient decrease in contractile force followed by a sustained increase. The negative and positive responses were antagonized by atropine and propranolol, respectively, but not by histamine antagonists terfenadine, cimetidine or thioperamide. Acetylcholine produced positive inotropic responses in the embryo while negative responses were observed after hatching. In myocardium of hatched chicks, compound 48/80, which releases histamine from mast cells, produced a transient decrease in contractile force followed by a sustained increase with a similar magnitude and time course to the case of exogenously applied histamine. The negative and positive responses were inhibited by atropine and propranolol, respectively, but not by terfenadine, cimetidine or thioperamide, which was similar to the case with the responses to histamine. The present results suggest that histamine, either applied exogenously or released from myocardial store sites, produces negative and positive inotropic responses in hatched chick myocardium which are due to release of acetylcholine and norepinephrine, respectively, from autonomic nerve terminals.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: Skinned fibres ; Myocardium ; Ryanodine receptor ; Ca2+ release ; Sarcoplasmic reticulum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), which is reported to inhibit the release of intracellularly stored Ca2+ in skeletal and smooth muscles, were examined in ventricular myocardia of the adult rat. In skinned papillary muscle fibres with functional sarcoplasmic reticulum (SR) preserved, application of 100 or 300 μM TMB-8 during the Ca2+ loading period had no significant effect on the peak tension of subsequent caffeine-induced contraction, but when applied during exposure to caffeine, concentration-dependent reduction of the peak tension was observed. At 1000 μM, TMB-8 reduced the peak tension of caffeine-induced contraction when applied either during Ca2+ loading or during exposure to caffeine. TMB-8 had no substantial influence on the Ca+-tension of skinned fibres without functional SR. In isolated papillary muscle preparations, TMB-8 prolonged the action potential duration and decreased the maximum rate of rise of potential, leading to abolition of contraction at 100 μM. In conclusion, TMB-8 may be a useful pharmacological tool for inhibiting Ca2+ release from SR, but only in skinned myocardial preparations.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    ISSN: 1432-1912
    Keywords: Key words Skinned fibres ; Myocardium ; Ryanodine receptor ; Ca2+ release ; Sarcoplasmic reticulum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), which is reported to inhibit the release of intracellularly stored Ca2+ in skeletal and smooth muscles, were examined in ventricular myocardia of the adult rat. In skinned papillary muscle fibres with functional sarcoplasmic reticulum (SR) preserved, application of 100 or 300 μM TMB-8 during the Ca2+ loading period had no significant effect on the peak tension of subsequent caffeine-induced contraction, but when applied during exposure to caffeine, concentration-dependent reduction of the peak tension was observed. At 1000 μM, TMB-8 reduced the peak tension of caffeine-induced contraction when applied either during Ca2+ loading or during exposure to caffeine. TMB-8 had no substantial influence on the Ca2+-tension of skinned fibres without functional SR. In isolated papillary muscle preparations, TMB-8 prolonged the action potential duration and decreased the maximum rate of rise of potential, leading to abolition of contraction at 100 μM. In conclusion, TMB-8 may be a useful pharmacological tool for inhibiting Ca2+ release from SR, but only in skinned myocardial preparations.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
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