The development of
ischemic contracture in rat was evaluated in relation to glycolytic production of
ATP and Ca2+ homeostasis. When the rate of glycolysis was reduced by
glycogen depletion (swimming at 33 degrees C for 2 h, administration of
isoprenaline or heart perfusion with it), the rate of
ischemic contracture development increased.
Isoprenaline increased the development of
contracture in a dose-dependent manner, and
dexamethasone potentiated the effect of
isoprenaline. The decrease in the intensity of
ATP/P1 exchange, probably reflecting the intensity of glycolytic phosphorylation of
ADP, which, in our conditions, arose from
ATP hydrolyzed mostly by Ca2+-
ATPase and Na, K-
ATPase, correlated with the development of
ischemic contracture. Experiments with the rapid equilibration of the extracellular compartment with Ca2+ in various concentrations in the presence or absence of
verapamil suggest that the development of
ischemic contracture depends on the rate of Ca2+ accumulation in myoplasm. This rate of Ca2+ accumulation correlates with the rate of glycogenolysis and glycolysis which seems to produce
ATP for active transport of
cations.