CARDIAC CONTRACTION AND INTRAMYOCARDIAL VENOUS-PRESSURE GENERATION IN THE ANESTHETIZED DOG

1. Two hypotheses relating to the influence of contraction of the heart on coronary venous pressure (P-v) were tested. The first assumes a direct transmission of left ventricular pressure (P-LV). According to the alternative hypothesis the P-v is caused by cyclical changes in the elastance of the surrounding tissue. 2. A small epicardial vein was cannulated retrogradely in eight open-chest dogs deeply anaesthetized with fentanyl. The duration of diastoles was varied after induction of a heart block with formaldehyde. Coronary arterial inflow and perfusion pressure mere controlled by a perfusion system connected to the left main coronary artery by a Gregg cannula. Stopped-flow P-v was studied with intrinsic coronary tone (IT) and after maximal dilatation with adenosine. 3. The P-v pulse in the first contraction after a long diastole was not significantly correlated to the P-LV pulse, with a slope of 0.5, in any dog, either with IT or during adenosine treatment. Comparing the first contraction after the long diastole with the last beat before, systolic P-v pulse decreased significantly in seven out of eight dogs, but systolic P-LV pulse increased in five dogs and was unaltered in three dogs in both conditions. In contrast, end-diastolic P-v was significantly correlated to the systolic P-v in each individual animal under either condition. 4. The results indicate that pressure generation in the small coronary veins can be explained on the basis of the time-varying elastance hypothesis and that a direct transmission of P-LV to P-v is absent.