Volume characteristics of extra- and intraparenchymal segments of the canine pulmonary artery.
The volumes of the extraparenchymal segment (VpaEP) and intraparenchymal segment (VpaIP) of the pulmonary arterial tree were determined in intact anesthetized dogs during room air breathing and acute hypoxia. Total pulmonary arterial blood volume (Vpatotal) was calculated as the product of pulmonary blood flow and pulmonary arterial circulation time. An angiographic technique was used to estimate VpEP. VpaIP was calculated by subtracting VpaEP from Vpatotal. During room air breathing at functional residual capacity, mean +/- SD of VpaEP was 17.1 +/- 5.1 ml and of VpaIP was 31.7 +/- 20.8 ml, representing 40% and 60%, respectively, of Vpatotal. Vpatotal increased 22.2 +/- 10.5 ml during lung inflation, with proportional increases in VpaIP and VpaEP. VpaEP was found to be influenced equally by changes in transmural pulmonary arterial and transpulmonary pressures. Acute hypoxia was accompanied by an increase in pulmonary vascular resistance and a decrease in volume distensibility of the extraparenchymal segment. Vpatotal increased 76% without changes in the relative volume distribution of VpaEP and VpaIP. These findings can be best explained by active vasomotion with an increase in down-stream pulmonary vascular resistance.
Volume characteristics of extra- and intraparenchymal segments of the canine pulmonary artery. The volumes of the extraparenchymal segment (VpaEP) and intraparenchymal segment (VpaIP) of the pulmonary arterial tree were determined in intact anesthetized dogs during room air breathing and acute hypoxia. Total pulmonary arterial blood volume (Vpatotal) was calculated as the product of pulmonary blood flow and pulmonary arterial circulation time. An angiographic technique was used to estimate VpEP. VpaIP was calculated by subtracting VpaEP from Vpatotal. During room air breathing at functional residual capacity, mean +/- SD of VpaEP was 17.1 +/- 5.1 ml and of VpaIP was 31.7 +/- 20.8 ml, representing 40% and 60%, respectively, of Vpatotal. Vpatotal increased 22.2 +/- 10.5 ml during lung inflation, with proportional increases in VpaIP and VpaEP. VpaEP was found to be influenced equally by changes in transmural pulmonary arterial and transpulmonary pressures. Acute hypoxia was accompanied by an increase in pulmonary vascular resistance and a decrease in volume distensibility of the extraparenchymal segment. Vpatotal increased 76% without changes in the relative volume distribution of VpaEP and VpaIP. These findings can be best explained by active vasomotion with an increase in down-stream pulmonary vascular resistance.