Abstract
At constant pressure work there was an increase in the oxygen consumption of the dog heartlung preparation after tachycardia due to auricular stimulation and a far greater increase in consumption after ouabain-induced ventricular tachycardia, as compared with control hearts beating at their own sinus rhythm. In neither condition was the increase in coronary flow greater than the spontaneous increase in the controls. It is suggested that an increase in oxygen demand, under certain circumstances, may be met primarily by an increased desaturation of coronary blood. "Therapeutic" doses of ouabain did not improve the mechanical efficiency of the preparation. "Toxic" doses of ouabain which gave rise to ventricular tachycardia did not decrease the phosphocreatine or labile nucleotide phosphorus content of the heart provided there was no hypoxia of the heart muscle.