title: The longitudinal distribution of pulmonary vascular resistance during unilateral hypoxia.
abstract: Pulmonary capillary hydrostatic pressure and the longitudinal distribution of pulmonary vascular resistance (arterial and venous components) can be determined by analysis of pressure decay curves following pulmonary artery occlusion. To validate this technique in intact animals, pulmonary artery occlusion pressure decay curves were obtained from both lungs in six anesthetized sheep during control conditions (100% O2) and during unilateral hypoxic ventilation (100% O2 versus 100% N2). Analysis of pulmonary artery occlusion pressure curves indicated the following: 1) in the hypoxic lung, unilateral hypoxia increased the precapillary portion of pulmonary vascular resistance from 72% of the total resistance to 89% of the total resistance in that lung; 2) in the nonhypoxic lung, unilateral hypoxia did not significantly affect the distribution of pulmonary vascular resistance; and 3) unilateral hypoxia produced no significant change in pulmonary capillary pressure in the hypoxic lung compared with control; however, pulmonary capillary pressure was significantly greater in the nonhypoxic lung. These results are consistent with other evidence that hypoxic pulmonary vasoconstriction acts locally and primarily affects resistance at the arteriolar level. Pulmonary artery occlusion pressure decay curve analysis appears to be a valid technique for the measurement of pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in intact anesthetized animals. These measurements pertain only to the vasculature distal to the site of pulmonary artery occlusion with the catheter, and, thus, caution must be used when applying this technique in a setting of nonhomogenous lung injury.
authors.affiliation: Department of Anesthesia, Stanford University School of Medicine, California 94305.
authors.forename: L C
authors.initials: LC
authors.lastname: Siegel
authors.forename: R G
authors.initials: RG
authors.lastname: Pearl
authors.forename: S L
authors.initials: SL
authors.lastname: Shafer
authors.forename: A K
authors.initials: AK
authors.lastname: Ream
authors.forename: R C
authors.initials: RC
authors.lastname: Prielipp
mesh_terms: D000818:Animals; D002302:Cardiac Output; D000860:Hypoxia / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D011651:Pulmonary Artery / Q000503:physiopathology*; D011669:Pulmonary Wedge Pressure; D012121:Respiration, Artificial / Q000379:methods; D012756:Sheep; D013815:Thermodilution; D014655:Vascular Resistance; D014661:Vasoconstriction