Acute effects of isoproterenol on cellular autophagy. Inhibition in myocardium but stimulation in liver parenchyma.

The influence of isoproterenol (IPR) on cellular autophagy was examined in left ventricular myocardium and in liver parenchyma of rats two hours after a subcutaneous injection of a low dose (3 mg/kg body weight). 4 animals were treated with IPR, 4 controls received Ringer solution. The average cytoplasmic volume fraction of the autophagic vacuoles (AV) was 1.6 X 10(-4) in the heart muscle of the controls. After treatment with IPR this value was reduced by 70% to 0.5 X 10(-4). This inhibition of cellular autophagy is interpreted as an initial anticatabolic reaction which might be responsible for the myocardial hypertrophy after chronic administration of IPR. An opposite influence of IPR was observed in the hepatocytes. The volume fraction of AV's increased twofold to 8.7 X 10(-4) after IPR, compared to 4.0 X 10(-4) in control animals. In the controls, the volume fraction of AV's in heart muscle was 57% of the value found in the liver. Comparing liver tissue after fixation by immersion and by perfusion, no statistically significant differences in the volume fractions and in the numerical densities of AV's were observed.