1 Division of Pediatric Cardiology, University of Washington School of Medicine, Seattle, Washington; Department of Medicine, The Peruvian University of Medical and Biological Sciences, Lima, Peru
2 Division of Pediatric Cardiology, University of Washington School of Medicine, Seattle, Washington
The diameter, distending pressure and flow in the superior vena cava and aortic flow were recorded simultaneously in unanesthetized dogs. Atrial systole produced a regurgitant flow pulse and an increase in pressure and diameter. Ventricular systole produced a sharp decrease in caval diameter and a large increase in flow. A second flow pulse occurred during ventricular diastole. Inspiration accelerated flow in the cava. During exercise, the caval diameter invariably decreased. Venoconstriction, however, could be unequivocally demonstrated in only 26% of the treadmill runs. In 88% of 33 recorded treadmill runs, the flow in the vena cava increased before the heart rate increased which, in turn, preceded the increase in aortic stroke volume. Frightening the animal produced a prompt decrease in caval diameter and distending pressure; this gave way to increased pressure, but without a corresponding increase in diameter. Epinephrine and norepinephrine produced a sustained increase in distending pressure and an initial decrease and a more sustained increase in diameter. Isoproterenol produced tachycardia and a decrease in distending pressure and diameter. Acetylcholine caused an initial bradycardia which was associated with an increase in diameter and pressure in the vena cava followed quickly by prolonged tachycardia which was associated with a decrease in pressure and diameter.
Accepted on January 10, 1966
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