I. Vergroesen et al., CARDIAC CONTRACTION AND INTRAMYOCARDIAL VENOUS-PRESSURE GENERATION INTHE ANESTHETIZED DOG, Journal of physiology, 480, 1994, pp. 343-353
1. Two hypotheses relating to the influence of contraction of the hear
t on coronary venous pressure (P-v) were tested. The first assumes a d
irect transmission of left ventricular pressure (P-LV). According to t
he alternative hypothesis the P-v is caused by cyclical changes in the
elastance of the surrounding tissue. 2. A small epicardial vein was c
annulated retrogradely in eight open-chest dogs deeply anaesthetized w
ith fentanyl. The duration of diastoles was varied after induction of
a heart block with formaldehyde. Coronary arterial inflow and perfusio
n 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 a
denosine. 3. The P-v pulse in the first contraction after a long diast
ole was not significantly correlated to the P-LV pulse, with a slope o
f 0.5, in any dog, either with IT or during adenosine treatment. Compa
ring the first contraction after the long diastole with the last beat
before, systolic P-v pulse decreased significantly in seven out of eig
ht dogs, but systolic P-LV pulse increased in five dogs and was unalte
red in three dogs in both conditions. In contrast, end-diastolic P-v w
as significantly correlated to the systolic P-v in each individual ani
mal under either condition. 4. The results indicate that pressure gene
ration in the small coronary veins can be explained on the basis of th
e time-varying elastance hypothesis and that a direct transmission of
P-LV to P-v is absent.