Energy dissipation and pulse wave attenuation in the canine carotid artery.
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Biomedical subjects
Publications and source records attributed to C D Bertram.
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Vein flow in the large extraparenchymal pulmonary veins is pulsatile and its wave form has an inverse relationship to left atrial pressure. Extraparenchymal pulmonary veins are thin walled and collapsible. This enables them to behave as highly compliant structures. Dimensional measurements of their cross sectional area in living open chested dogs showed them to be non circular at low left atrial pressures. They rapidly assumed a circular cross section as left atrial pressure rose. Only at pressures above 1.5 kPa (11 mmHg) were the pulmonary veins circular in cross section. The aggregate volume of the large extraparenchymal pulmonary veins, when fully distended, was found to be equal to or greater than one stroke volume of the heart. The extraparenchymal pulmonary veins act as a reservoir to the left atrium so that left ventricular stroke volume can be maintained relatively unaffected by beat by beat changes in right ventricular stroke output. Their behaviour at normal mean left atrial pressures also enables them to isolate the lung capillaries from retrograde transmission of positive pressure transients from the left atrium, which could otherwise impede venous outflow of blood from the lung capillary bed.
The influence of arterial dimensions and viscoelasticity on pulse wave propagation has been expressed in many theoretical models of blood flow in arteries, but few experimental tests of these theories in vivo have been reported. The measurements required for such tests include not only the arterial viscoelasticity, diameter, and wall thickness, but also the true propagation coefficients and impedances, for comparison with the values "predicted" by solution of the model equations. We made such measurements in 16 experiments on the femoral artery in nine anesthetized dogs. A two-point pressure and flow technique was used to measure wave propagation, and an ultrasonic micrometer was used to measure vessel diameter as a function of time and pressure. Measured attenuation constants ranged from 0.010 at 1.3 Hz to 0.075 at 12.7 Hz, and were more than twice as large as those predicted by two representative linear models. True phase velocity, which increased from 6.71 m/sec at 1.3 Hz to 10.54 m/sec at 12.7 Hz, agreed closely with the values computed by the Cox model but were lower than those given by the Jager model. The resistive, but not the reactive, component of longitudinal impedance was significantly greater than predicted by the models at all frequencies. The experiments do not identify the source of these discrepancies. The use of linear models to calculate pulsatile blood flow from pressure gradients in relatively small vessels, or to calculate attenuation and characteristic impedance from arterial viscoelasticity in vessels of any size, produces significant errors.
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