title: Pulmonary capillary pressure measurement during global hypoxia in sheep.
abstract: Analysis of the pressure decay following pulmonary artery occlusion can be used to determine pulmonary capillary pressure and to calculate the magnitudes of the arterial and venous components of pulmonary vascular resistance. The separation of pulmonary vascular resistance into components has been termed "the longitudinal distribution of pulmonary vascular resistance" to emphasize the fact that different pressures occur at a number of sites in the pulmonary circulation. The longitudinal distribution of pulmonary vascular resistance is closely related to pulmonary capillary pressure. Several methods of data analysis have been proposed to determine pulmonary capillary pressure from the pressure decay following pulmonary artery occlusion. In this study, three methods of data analysis were applied to the model of hypoxic pulmonary vasoconstriction to evaluate the validity of the methodology in a well known model. Pulmonary artery occlusion pressure decay curves were obtained from eight halothane-anesthetized sheep during control conditions (FIO2 = 0.99) and during hypoxic ventilation (FIO2 = 0.14). Analysis of the pulmonary artery occlusion pressure decay curves indicated the following results: 1) Hypoxia increased mean pulmonary artery pressure by 105% and increased pulmonary vascular resistance by 149%; 2) the increase in the calculated arterial component of pulmonary vascular resistance accounted for 88% of the increase in pulmonary vascular resistance with hypoxia; and 3) hypoxia produced only a 1.0 mm Hg increase in pulmonary capillary pressure. These results are consistent with other evidence showing that hypoxia primarily produces precapillary pulmonary vasoconstriction and has little effect on pulmonary capillary pressure. Pulmonary artery occlusion pressure decay curve analysis appears to be a valid technique for the measurement of pulmonary capillary pressure during hypoxia in intact anesthetized animals.
authors.affiliation: Department of Anesthesia, Stanford University School of Medicine, California.
authors.forename: L C
authors.initials: LC
authors.lastname: Siegel
authors.forename: R G
authors.initials: RG
authors.lastname: Pearl
authors.forename: D A
authors.initials: DA
authors.lastname: August
mesh_terms: D000818:Animals; D002200:Capillary Resistance; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D011651:Pulmonary Artery / Q000503:physiopathology; D011652:Pulmonary Circulation; D011669:Pulmonary Wedge Pressure; D012756:Sheep; D014655:Vascular Resistance