title: Mechanical factors do not influence blood flow distribution in atelectasis.
abstract: The contribution of mechanical factors to the vascular resistance of the atelectatic lung has been studied in vivo in the anesthetized open-chest dog. When the left lung was ventilated with an hypoxic gas mixture (while the right lung was ventilated with 100% O2), left lung blood flow decreased from 0.99 +/- 0.11 1.min-1 to 0.40 +/- 0.08 1.min-1 due to hypoxic pulmonary vasoconstriction (hypoxic stimulus PSO2 = 36.1 +/- 0.8 mmHg). When the left lung was made atelectatic, blood flow decreased to 0.65 +/- 0.11 1.min-1, consistent with a weaker hypoxic stimulus (PSO2 = 54.0 +/- 3.2 mmHg). With the addition of sodium nitroprusside infused intravenously, left lung blood flow increased to 1.05 +/- 0.14 1.min-1 during atelectasis, and to 0.61 +/- 0.09 1.min-1 during hypoxic ventilation, while flow remained at 0.94 +/- 0.18 1.min-1 during hyperoxic ventilation. When the results were plotted on pressure-flow diagrams, the hyperoxic, hypoxic, and atelectatic lung points fell on the same pressure-flow line in the presence of nitroprusside. It is concluded that hypoxic pulmonary vasoconstriction is the major (but not necessarily only) determinant of increased vascular resistance in the atelectatic lung, and that passive mechanical factors do not measurably affect blood flow distribution during open-chest atelectasis.
authors.affiliation: Department of Anesthesia, University Hospital, Lund, Sweden.
authors.forename: F L
authors.initials: FL
authors.lastname: Miller
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: G
authors.initials: G
authors.lastname: Malmkvist
authors.forename: C
authors.initials: C
authors.lastname: Marshall
authors.forename: B E
authors.initials: BE
authors.lastname: Marshall
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D004285:Dogs; D005260:Female; D000860:Hypoxia / Q000503:physiopathology; D008168:Lung / Q000187:drug effects / Q000503:physiopathology; D009599:Nitroprusside / Q000494:pharmacology; D010100:Oxygen / Q000008:administration & dosage; D001261:Pulmonary Atelectasis / Q000503:physiopathology*; D011652:Pulmonary Circulation / Q000187:drug effects; D012121:Respiration, Artificial / Q000379:methods; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D009599:Nitroprusside; D010100:Oxygen