1. Two hypotheses relating to the influence of contraction of the heart on coronary venous pressure (Pv) were tested. The first assumes a direct transmission of left ventricular pressure (PLV). According to the alternative hypothesis the Pv 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 were controlled by a perfusion system connected to the left main coronary artery by a Gregg cannula. Stopped-flow Pv was studied with intrinsic coronary tone (IT) and after maximal dilatation with adenosine. 3. The Pv pulse in the first contraction after a long diastole was not significantly correlated to the PLV 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 Pv pulse decreased significantly in seven out of eight dogs, but systolic PLV pulse increased in five dogs and was unaltered in three dogs in both conditions. In contrast, end-diastolic Pv was significantly correlated to the systolic Pv 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 PLV to Pv is absent.
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