Changes in oxidative metabolism and myocardial blood flow were investigated in adult greyhounds following transthoracic shocks from a DC cardiac defibrillator (400 Joules stored energy, damped sine wave, 0·5 min intervals). Myocardial lactate extraction became negative maximally at 1 min, following both two (mean -24%±SEM24) or five ( -193%±148) shocks and returned to baseline by 6-15 min. Transient reductions were also observed in myocardial extraction of pyruvate and free fatty acids but not glucose. Myocardial necrosis assessed at 4 h following the shocks was 005 g (±0·03) after two shocks, 6·5 g (±1·5) after five shocks and zero in controls. Mean peak noradrenaline levels in arterial (785±319 pg . ml-1) and coronarv sinus (916±313 pg . ml-1) blood at 1 min after five shocks were higher than after 0 shocks (82±33 pg. ml-1) and 201±63 pg . ml-1)respectively), P<0·05.Great cardiac venous blood flow was measured by a thermodilution technique, with continuous infusion of 0·9% saline, before, during and after five shocks. Mean bloodflowfellfrom 47±13 ml. min-1) to a minimum of 36±7 ml. min-1) during shocks, and then rose to 83±17 ml. min-1) at 2 min after the fifth shock (P<0·05).Following damaging counter shocks, oxidative metabolism is depressed, in keeping with a primary disturbance of mitochondrialfunction. These metabolic changes are not secondary to ischaemia, since an increase in blood flow in the great cardiac vein (GCV) is observed. Vasodilatation of the coronary vascular bed must occur to account for this. © 1992 The European Society of Cardiology.