Effect of Starvation on Contractile Response of Isolated Rat Atria to Citrate and Bicarbonate-Free Medium

Isolated atria from 24-hr starved rats show a smaller rate of decline of contractility with time, when incubated in the absence of exogenous substrate than atria from fed rats. During starvation, endogenous substrate apparently accumulates and can be used by the heart to maintain contractility in vitro. The nature of this endogenous substrate was elucidated by the use of bicarbonate-free medium and 1.5 mM citrate. These agents apparently depress contractility by an inhibition of the phosphofructokinase (PFK) reaction in the glycolytic cycle. Both inhibitors produced marked, but not complete, contractile depression of atria from starved or fed rats incubated in the absence of exogenous substrate. This depression is likely due to an interference with the utilization of endogenous substrate, probably glycogen, normally metabolized via PFK. The maintenance of some degree of contractility in the presence of these inhibitors indicates that endogenous substrates, not metabolized via PFK, are utilized. Addition of 20 mM glucose to atria from fed or starved rats incubated in substrate-free medium resulted in a marked positive inotropic effect in both cases. This may indicate that glycolytic enzymes are present and functional after 24 hr of starvation.