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Protection against cardiac anoxia — role and limitations of increased glycogen reserves in the isolated rat right ventricular strip

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Summary

The effects of drugs on rat cardiac glycogen reservesin vivo, and on the subsequentin vitro sensitivity of the right ventricular strip preparation to anoxia have been investigated.

Isoproterenol (0.2 mg/kg i.p.) causes immediate cardiac stimulation and reduction of glycogen reserves, coupled with an increased susceptibility to anoxia. Several hours after administration, glycogen levels are found to be greatly (100–200%) increased, by a “supercompensation” mechanism, and a marked tolerance to anoxia can be simultaneously demonstrated.

In contrast, large doses of corticosteroids (dexamethasone, 8 mg/kg i.m.) increase glycogen levels without initial stimulation and glycogen depletion; increased myocardial tolerance to anoxia parallels the increase in glycogen reservesin vivo.

We conclude that the myocardial tolerance to anoxia in this model is related to increased glycogen reserves, which increase the rate and/or duration of anaerobic glycolysis during anoxia.

Zusammenfassung

Es wurde untersucht, ob Substanzen, die unter geeigneten Versuchsbedingungen an der Ratte in vivo die myokardialen Glykogenreserven erhöhen, in vitro bei Anoxie die Widerstandsfähigkeit vom Muskelstreifen des rechten Ventrikels zu steigern vermögen.

Isoproterenol (0,2 mg/kg i.p.) bewirkt an Ratten starke kardiale Stimulierung und Reduktion der myokardialen Glykogenreserven, verbunden mit gesteigerter Empfindlichkeit gegenüber Anoxie. Mehrere Stunden nach der Applikation sind die myokardialen Glykogenkonzentrationen erheblich erhöht (um 100–200%) durch einen „Kompensationsmechanismus”. Die Herzmuskelstreifen derartig behandelter Tiere zeigten deutlich Anoxietoleranz.

Hohe Dosen von Kortikosteroiden, wie z. B. Dexamethason (8 mg/kg i.m.), bewirken gleichfalls einen Anstieg der myokardialen Glykogenkonzentration, jedoch ohne vorhergehende Stimulierung der Herzen und Abfall des Glykogengehaltes. Die myokardiale Widerstandsfähigkeit bei Anoxie, geprüft an den Herzmuskelstreifen, ist parallel zu dem Anstieg der Glykogenreserven erhöht.

Es ist hieraus zu schließen, daß die myokardiale Anoxietoleranz in dem vorliegenden Untersuchungsmodell von der Höhe der Glykogenreserven im Herzen abhängt, die während der Anoxie maßgebend sind für die Stärke und Dauer der anaeroben Glykolyse im Herzen.

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Dedicated to Prof. Dr. Grünewald on the occasion of his 60th birthday.

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Towart, R., Schloßmann, K. & Kazda, S. Protection against cardiac anoxia — role and limitations of increased glycogen reserves in the isolated rat right ventricular strip. Basic Res Cardiol 76, 639–646 (1981). https://doi.org/10.1007/BF01908054

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