The effects of acute systemic anoxia on blood pressure and flow in the coronary sinus were investigated in 23 anaesthetized open-chest dogs. Severe anoxia, produced by inhalation of 100°/0 nitrogen over a period of 1.5 to 2 rain, elicited regularly a progressive rise in amplitude of pressure pulsations within the coronary sinus. It amounted at the height of anoxia to 37.3 mm Hg, on the average, as compared to 5.3 mm Hg under control conditions (~ 600O/o). Similarly, the mean coronary sinus pressure rose progressively during anoxia. The rise in coronary sinus pressure paralleled the increase of coronary sinus outflow and ventrieular contractile force. It evidently preceded the onset of anoxie bradycardia. Bilateral vagotomy, which caused attenuation or abolition of bradycardia, reduced only moderately anoxic rise in coronary sinus pressure. It is concluded that the rise in the amplitude of pressure pulsations in the coronary sinus, encountered in acute systemic anoxia, is due to the increase of ventricular contractile force, and, particularly, to the improved filling of the coronary veins, correlated with the augmentation of coronary blood flow. Anoxic bradycardia is an additional factor contributing to the increased venous filling by prolonging the duration of the filling period. * Death by accident in March 23, 1966. ** This study was performed during the tenure of a stipend from the Ministry of Health of the German Democratic Republic.