1. Experiments were undertaken on strips of human atrial and ventricular muscle, on right ventricular rabbit papillary muscles and on the rabbit interventricular septum. 2. In all preparations an increase of developed tension after 30 min exposure to ouabain was apparent only at or above a concentration of 10 −7 mol/l (73 μg/l). 3. In the rabbit septum there was a net loss of potassium on exposure to ouabain if the concentration was greater than 10 −7 mol/l. There was no net loss, or gain, of potassium at lower concentrations. Loss of potassium, indicating inhibition of the sodium pump, could not be dissociated from the positive inotropic effect of ouabain. 4. The greater sensitivity to ouabain of human myocardium in vivo (10 −8 mol/l) than in vitro (10 −7 mol/l) may be due to cellular changes occurring in isolated preparations.

1. We have studied the acute effects of frusemide, triamterene and amiloride on potassium exchange, the action potential and mechanical function of isolated rabbit myocardium. 2. Potassium exchange in the myocardium was unaltered by these diuretics. 3. Frusemide and amiloride did not affect the action potential of rabbit papillary muscles. Triamterene caused a transient shortening of the action potential. 4. Frusemide and triamterene did not alter myocardial mechanical function in rabbit papillary muscles or the interventricular septum. Amiloride caused a reduction of about 5% in developed tension in two out of three papillary muscles.

1. The efflux of 14 C-Iabelled 5,5-dimethyl-2,4-oxazolidinedione (DMO) from the myocardium of the rabbit has been studied. The perfusate pH was 7·38. 2. The effluent curve is complex and appears to be the resultant of movement between at least four compartments. 3. The first two probably represent intravascular and extracellular compartments; the last two have smaller rate constants and may represent intracellular spaces. Intracellular pH (pH 1 ) calculated from the effluent curve was 7·23 ± 0·05. pH 1 estimated from the steady-state distribution volume of DMO was 7·28 ± 0·02. 4. The existence of two intracellular compartments suggests that DMO is not homogeneously distributed in the myocardium. It is suggested that the apparent greater buffering capacity of cardiac than skeletal muscle can be explained by the greater number and volume of mitochondria in the myocardium, compartmentalization of DMO and assumptions inherent in the DMO method for the measurement of pH 1 .

1. The rebreathing and steady-state methods for assessing the response to inhaled carbon dioxide were compared in six normal subjects under control conditions and during metabolic acidosis and alkalosis. 2. The slopes of the CO 2 response lines obtained with the two methods under control conditions were not significantly different. 3. Metabolic acidosis and alkalosis produced a significant change in the intercept of the response line when this was assessed with the steady-state technique. The slope of the response lines did not change significantly in alkalosis but there was probably a small increase during acidosis. 4. Using the rebreathing technique there was no significant change in intercept in acidosis and alkalosis, but the slope varied significantly from control values. 5. It is concluded that the two methods of assessing the respiratory response to inhaled CO 2 are comparable under normal acid-base conditions. This similarity does not hold in metabolic changes of the acid-base state.

1. The pattern of urinary acid excretion during mannitol diuresis was studied in five normal adult subjects. 2. At peak diuresis (osmolal clearance 19·3–27·9 ml/min), the urinary pH approached 6·9 irrespective of the initial pH. 3. Total hydrogen ion excretion fell sharply during mannitol diuresis. Changes in the excretion of ammonium and titratable acid were small and variable, but in each subject bicarbonate excretion increased markedly. 4. Despite previous conflicting published results urinary acid excretion during mannitol diuresis in man resembles that in the dog and is dominated by a bicarbonate diuresis.