1. Flounder hearts were cannulated in apparatus where input and output pressures could be altered. Output of spontaneously beating hearts was seen to be dependent upon input filling pressure. 2. Heart output remained constant between 10 and 20°C but above this temperature output fell. This was seen to be a consequence of reduction in the rate of contraction despite increasing stroke volume. 3. In the presence of adrenaline heart rate was greater at 10 and 20°C than in control hearts. Stroke volume was however reduced in the presence of adrenaline and overall output was only greater in adrenaline-treated hearts at 10°C. 4. In paced atrial and ventricular strips an increase in temperature from 10°C to 20°C greatly reduced contractile force. In the presence of 1 μM adrenaline at 10°C contractile force was increased above control values. At 20°C 1 μM adrenaline increased contractile force in atrial and ventricular strips although contractile force failed to reach that seen in 10°C controls. 5. While total cardiac output was unchanged between 10 and 20°C autoregulation could not be maintained above this temperature range.