Effect of anoxia on isolated turtle tissues: is the response to anoxia mediated by protein kinase second messengers?

Organ slices from the turtle Trachemys scripta elegans were incubated under aerobic and anoxic conditions to examine the effect of protein kinase (PrK) second messengers in potentiating the biochemical responses to anoxia exposure. Incubating liver slices from aerobic animals under anoxic conditions produced biochemical changes exactly similar to those observed in vivo: phosphofructokinase (PFK) was more sensitive to citrate inhibition and the percentage of glycogen phosphorylase (GP) in the active a form increased. On the other hand, incubating brain and heart tissue slices under anoxic conditions produced no changes in PFK and GP kinetic constants. Addition of PrK second messengers (dibutyryl-cAMP or Ca2+ plus phorbol myristate acetate) to the incubated tissues did not promote anoxia-associated changes in aerobically incubated tissues nor did they prevent anoxia-associated changes in anaerobically incubated tissues. These results suggest that unidentified external hormonal signals mediate heart and brain responses to anoxia. It is also apparent that cAMP and Ca2+ plus phospholipid do not play a role in bringing about the anoxia-induced changes in PFK, GP and fructose 2,6-bisphosphate in liver of turtles.