The effects of drugs on rat cardiac
glycogen reserves in vivo, and on the subsequent in 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 reserves in 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.