Preparation of a nuclear membrane fraction from normal and from herpes virus-infected BHK cells.

decreased until the beat rate was apparentlyrestored to near-normal, all waves then being of reduced amplitude. The mean pressure gradually declined. This progressive loss of contractile force preceded complete cessation of work within 90min in hearts which were not terminated experimentally within this time. Normal concentrations of ATP and phosphocreatine were maintained despite the work failure. Total lactate production was not greater than in normal working hearts, although the Daunorubicin-toxic hearts has increased intracellular lactate concentrations. Clinically, the value of digitalis compounds in patients suffering Daunorubicininduced cardiac abnormalities has been considered (Lefrak et al., 1973; Al-Ismail et al., 1977). However, these authors present an inconclusive picture. In the present study we have observed a protective effect of Digoxin when the drug was administered to animals before exposure of the hearts to Daunorubicin. Hearts from digitalized rats maintained control aortic pressure profiles and beat rate during a 45min perfusion with Daunorubicin at concentrations that in the absence of Digoxin produced work failure. This leads to the suggestion that Digoxin may be of value when given clinically before Daunorubicin.