title: Effects of active vasoconstriction and total flow on perfusion distribution in the rabbit lung.
abstract: We analyzed the effects of hypoxic vasoconstriction and total flow on the distribution of pulmonary perfusion in 38 isolated left rabbit lungs perfused under zone 3 conditions. Lungs were suspended in an upright position, oriented to the apicobasal line. Distributions of regional perfusion rates (RPR) along the vertical and horizontal axes were determined using nonradioactive microspheres labeled with heavy metal elements, which were detectable with X-ray fluorescence spectrometry. Changing the O2 concentration of a respirator and an extracorporeal membrane oxygenator independently, respective influences of active vasoconstriction induced by alveolar hypoxia and pulmonary artery hypoxia (PA hypoxia) on the RPR distribution were examined at a flow rate of 0.4 ml x min(-1) x g wet lung tissue(-1). To analyze the effects of changes in total flow, we investigated the RPR distribution at a perfusion rate of 1.2 ml x min(-1) x g wet lung tissue(-1). The RPR distribution in the absence of hypoxia was inhomogeneous and was augmented in the lower lung fields, whereas alveolar hypoxia shifted the RPR upward and significantly diminished the RPR in the lung base. RPR distributions along the horizontal axes under alveolar hypoxia conditions demonstrated that remarkable hypoxic pulmonary vasoconstriction (HPV) takes place in medial regions at the lung base. PA hypoxia altered the RPR distribution in qualitatively the same manner as alveolar hypoxia. Increased flow rate augmented the RPR in the lung, except in the dorsobasal region. These results suggest that the occurrence of HPV and the vascular conductance are not uniform throughout the lung.
authors.affiliation: Department of Medicine, School of Medicine, Keio University, Tokyo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Oyamada
authors.forename: M
authors.initials: M
authors.lastname: Mori
authors.forename: I
authors.initials: I
authors.lastname: Kuwahira
authors.forename: T
authors.initials: T
authors.lastname: Aoki
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: A
authors.initials: A
authors.lastname: Miyata
authors.forename: K
authors.initials: K
authors.lastname: Nishio
authors.forename: N
authors.initials: N
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Naoki
authors.forename: H
authors.initials: H
authors.lastname: Kudo
authors.forename: Y
authors.initials: Y
authors.lastname: Ohta
authors.forename: K
authors.initials: K
authors.lastname: Yamaguchi
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D000860:Hypoxia / Q000503:physiopathology; D066298:In Vitro Techniques; D008168:Lung / Q000502:physiology / Q000503:physiopathology; D008171:Lung Diseases / Q000503:physiopathology; D008297:Male; D008863:Microspheres; D010100:Oxygen; D010313:Partial Pressure; D011650:Pulmonary Alveoli / Q000503:physiopathology; D011651:Pulmonary Artery / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000502:physiology*; D011817:Rabbits; D012039:Regional Blood Flow; D015203:Reproducibility of Results; D014652:Vascular Diseases / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D010100:Oxygen