title: The vascular site of action of hypoxia in the neonatal pig lung.
abstract: To determine the vascular site(s) of action of hypoxia in the neonatal pig, isolated lungs were perfused at a constant flow rate and left atrial pressure; arterial, venous, and double occlusions were performed. The distribution of the total pulmonary vascular resistance and the total dynamic vascular compliance were calculated using a model of the pulmonary circulation consisting of upstream, central, and downstream compliances and resistances upstream and downstream of central compliance. In addition, the static vascular compliance was measured by venous followed by arterial occlusion, and the total vascular volume was measured by dye-dilution. In this preparation during control conditions alveolar PO2 = 12 +/- 2 kPa), total pulmonary vascular resistance was nearly evenly divided between resistance upstream and downstream of double occlusion pressure and total dynamic vascular compliance was concentrated mainly in the central compliance (7% upstream compliance, 82% central compliance, and 11% downstream compliance). Hypoxia (alveolar PO2 = 4 +/- 1 kPa) increased both resistance upstream of double occlusion pressure (p < 0.005) and resistance downstream of double occlusion pressure (p < 0.02) and decreased central compliance (p < 0.005). Hypoxia also decreased total pulmonary blood volume (p < 0.02). These results suggest that in the pulmonary vasculature of the neonatal pig, hypoxia results mainly in 1) arterial constriction as evidenced by a large increase in upstream resistance and a decrease in total pulmonary blood volume and 2) a smaller but significant venous constriction. This venous constriction may have implications in the pathogenesis and therapy of pulmonary vascular diseases associated with hypoxia such as postasphyxial lung disease and bronchopulmonary dysplasia.
authors.affiliation: Department of Pediatrics, Medical College of Wisconsin, Milwaukee 53226.
authors.forename: L D
authors.initials: LD
authors.lastname: Nelin
authors.forename: D A
authors.initials: DA
authors.lastname: Rickaby
authors.forename: J H
authors.initials: JH
authors.lastname: Linehan
authors.forename: C A
authors.initials: CA
authors.lastname: Dawson
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D003187:Compliance; D004548:Elasticity; D000860:Hypoxia / Q000150:complications / Q000503:physiopathology*; D066298:In Vitro Techniques; D010477:Perfusion; D011652:Pulmonary Circulation / Q000502:physiology*; D013552:Swine; D014652:Vascular Diseases / Q000209:etiology; D014655:Vascular Resistance / Q000502:physiology