Aim: To characterize the buffering function of the pulmonary artery in vivo and to determine the role of vascular smooth muscle (VSM) activation in vessel wall elasticity.
Material and method: Pulmonary artery pressure and diameter were measured in 9 anesthetized sheep. Pulmonary artery hypertension was induced by mechanical occlusion of the pulmonary artery and by phenylephrine infusion (5 microg/kg/min) (PHE). Once the pressure-diameter loop was obtained, hysteresis was reduced to a minimum by increasing the modulus of viscosity. Elasticity was calculated as the first derivative of mean diastolic pressure assuming a purely elastic relation. Pulse wave velocity (PWV) and time constant (tau) were also obtained.
Results: Systolic, diastolic, mean and pulse pressures were similar during pulmonary artery hypertension and PHE infusion, but significantly higher in comparison to baseline conditions. Elasticity and diameter of the pulmonary artery increased significantly. In contrast, during VSM activation elasticity remained unchanged and diastolic diameter was reduced. PWV increased during both pulmonary artery hypertension and PHE infusion (p < 0.05); however, the increase during PHE infusion was smaller (15%) than during induced hypertension (33%). tau was significantly reduced during hypertension, but did not change during VSM activation.
Conclusions: VSM activation may offset the deleterious effect of pulmonary artery hypertension on arterial wall stiffness by reducing elasticity and PWV. The VSM may modulate the Windkessel function in the pulmonary artery, preserving elasticity indexes during pulmonary artery hypertension.