http://link.springer.com/content/pdf/10.1007/978-3-642-45467-7_10.pdf

Basic Actions of Ions and Drugs on Myocardial High-Energy Phosphate Metabolism and Contractility

SummaryA single subcutaneous dose (1 mg/kg) of isoproterenol (ISO) increases the net calcium-45 uptake into the ventricular myocardium of normal rats by a factor of 4 within 6 hours. When the same dose of ISO was administered to rats with aortic constriction the rise in labelled Ca uptake by the hypertrophied myocardium of the left ventricle was greatly reduced. A decrease in ISO-induced Ca uptake also occurred in the non-hypertrophied right ventricular myocardium. Consequently, the stimulatory effect of ISO on the Ca-dependent high energy phosphate consumption was considerably diminished. A similar restriction of ISO-induced radiocalcium uptake and ATP utilization occurred in hypertrophied hearts of chronically ISO-treated rats or when the rats were exposed to other forms of experimental stress such as bleeding or cold. Although the ISO-induced cardiomegaly was reversed within 7 days, the insensitivity to β-adrenergic stimulation persisted for more than 3 weeks. The results indicate that the decrease in responsiveness to β-adrenergic agents is not due to the hypertrophy itself but must be considered to be an independent phenomenonpossibly resulting from adaptation to chronic β-adrenergic overstimulation.ZusammenfassungDie45Ca-Nettoaufnahme in das normale Rattenherz wird nach einer einmaligen subkutanen Gabe (1 mg/kg) von Isoproterenol (ISO) innerhalb von 6 Stunden auf das 4fache der Norm erhöht. Nach Erzeugung einer Herzhypertrophie (Aortenkonstriktion, chronische ISO-Verabreichung, Streßsituationen wie Kälte oder Entblutung) tritt jedoch Gewöhnung ein, so daß das Myokard nicht mehr auf dieses β-Rezeptoren-Stimulans reagiert. Dies zeigt sich darin, daß in hypertrophierten Herzen die45Ca-Nettoaufnahme unter dem Einfluß von 1 mg ISO/kg nicht mehr — wie normal — gesteigert werden kann und auch die ISO-stimulierte Abnahme von ATP und Kreatinphosphat ausbleibt. Die Einschränkung der β-adrenergen Stimulierbarkeit darf jedoch nicht als direkte Folge der Faserhypertrophie angesehen werden, da (1) auch das nicht-hypertrophierte rechte Ventrikelmyokard nach Aortenkonstriktion nur noch wenig auf ISO anspricht und (2) nach Absetzen der chronischen ISO-Vorbehandlung der Hypertrophie-Prozeß schneller zurückgebildet wird als die Hemmung der ISO-induzierten Radiocalcium-Aufnahme. Die Minderansprechbarkeit des Herzens auf injizierte β-adrenerge Katecholamine ist wahrscheinlich als Folge einer streßbedingten chronischen Überstimulation des Sympathikus anzusehen. Diese Einschränkung der sympathischen Stimulierbarkeit entwickelt sich gleichzeitig mit der Hypertrophie — aber unabhängig davon.

Restriction ofβ-adrenergic responsiveness in hypertrophied ventricular myocardium of rats@@@Einschränkung derβ-adrenergen Ansprechbarkeit im hypertrophierten Rattenmyokard

A single subcutaneous dose (1 mg/kg) of isoproterenol (ISO) increases the net calcium-45 uptake into the ventricular myocardium of normal rats by a factor of 4 within 6 hours. When the same dose of ISO was administered to rats with aortic constriction the rise in labelled Ca uptake by the hypertrophied myocardium of the left ventricle was greatly reduced. A decrease in ISO-induced Ca uptake also occurred in the non-hypertrophied right ventricular myocardium. Consequently, the stimulatory effect of ISO on the Ca-dependent high energy phosphate consumption was considerably diminished. A similar restriction of ISO-induced radiocalcium uptake and ATP utilization occurred in hypertrophied hearts of chronically ISO-treated rats or when the rats were exposed to other forms of experimental stress such as bleeding or cold. Although the ISO-induced cardiomegaly was reversed within 7 days, the insensitivity to β-adrenergic stimulation persisted for more than 3 weeks. The results indicate that the decrease in responsiveness to β-adrenergic agents is not due to the hypertrophy itself but must be considered to be an independent phenomenon — possibly resulting from adaptation to chronic β-adrenergic overstimulation.

Restriction of β -adrenergic responsiveness in hypertrophied ventricular myocardium of rats

In fruheren tier-experimentellen Studien von Fleckenstein, D00f6ring und Kammer,eier (1966, 1967, 1968) wurden 2 Typen von kontraktiler Herz-In-suffizienz herausgearbeitet: 

1.

Das Herzversagen infolge Mangels an energiereichem phosphat nach Hypoxie, Ischamie oder Hemmung des oxydativen Stoffwechsels;




2.

das Herzversagen infolge einer ungen00fcgenden Utilisation von energie-reichem Phosphat. Eine solche Utilisations-Insuffizienz tritt z. B. bei Ca++- Mangel ein, weil dann die Ca++-abhangige Myofibrillen–ATPase in den erregten Myokardfasern nicth mehr gen00fcgend ATP zur Gewinnung der Kontraktionsenergie spalten kann.

Einschränkung der Isoproterenol-induzierten 45Ca++-Netto-Aufnahme und der Utilisation von energiereichem Phosphat im hypertrophierten Rattenmyokard

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Einschränkung der Isoproterenol-induzierten 45Ca++-Netto-Aufnahme und der Utilisation von energiereichem Phosphat im hypertrophierten Rattenmyokard