Abstract

2-Deoxyglucose depresses atrial contractility without altering membrane potentials significantly, although the ATP level is progressively reduced. Pyruvate is able to counteract the 2-deoxyglucose depression only partially, indicating some relation between the Embden-Meyerhof pathway and contraction. Nevertheless, pyruvate elevates the ATP level above the control values. 2-Deoxyglucose depresses more rapidly in the absence of glucose. Addition of glucose restores the developed tension partially, indicating that contractility to some extent depends either on the initial phases of glucose metabolism, or on the operation of a nonglycolytic pathway, since there is evidence that 2-deoxyglucose blocks the Embden-Meyerhof pathway under these conditions.

Atrial rate is not altered by removal of exogenous glucose, is only slightly depressed by 2-deoxyglucose in glucose medium, but is markedly slowed by 2-deoxyglucose in the absence of glucose. Since pyruvate has only a limited ability to restore the depressed rate, the discharge of pacemaker calls is also related to glucose utilization.