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  • Title: Hypoxic pulmonary vasoconstriction in human lungs. A stimulus-response study.
    Author: Hambraeus-Jonzon K, Bindslev L, Mellgård AJ, Hedenstierna G.
    Journal: Anesthesiology; 1997 Feb; 86(2):308-15. PubMed ID: 9054249.
    Abstract:
    BACKGROUND: A stimulus-response relation between alveolar oxygen tension and pulmonary vascular resistance has been observed in animals. This study investigated this relation in healthy human lungs. The distribution of pulmonary blood flow was measured during unilateral (1) graded hypoxia (fractional concentration of oxygen in inspired gas [FIO2] = 0.12, 0.08, and 0.05) and contralateral hyperoxia (FIO2 = 1.0; n = 6); (2) single-step hypoxia (FIO2 = 0.05) and contralateral hyperoxia (n = 5); and (3) normobaric hyperoxia and contralateral normoxia (FIO2 = 0.25; n = 6). METHODS: Seventeen patients with healthy lungs were studied during intravenous anesthesia. The lungs were separately and synchronously ventilated. The relative perfusion of each lung was assessed by the inert gas (sulfurhexafluoride) elimination technique. RESULTS: (1) Unilateral graded hypoxia reduced the perfusion of the hypoxic lung from a mean (+/-SD) of 52 (2)% of cardiac output (Q) during bilateral hyperoxia, to 47 (5)% (P > 0.05) 40 (3)% (P < 0.01), and 30 (8)% (P < 0.001) of Q, respectively. These progressive reductions in the perfusion of the hypoxic lung were all significantly different from each other. (2) Unilateral single-step hypoxia caused a blood flow diversion of the same magnitude as when the lung was previously ventilated with FiO2 of 0.12 and 0.08. The perfusion of the hypoxic lung was reduced from 46 (9)% of Q (bilateral hyperoxia) to 26 (4)% of Q (P < 0.01). (3) Unilateral hyperoxia did not significantly change the relative blood flow distribution between the two lungs or the pulmonary artery pressure. CONCLUSIONS: A stimulus-response relation between graded hypoxia and blood flow diversion defines hypoxic pulmonary vasoconstriction in the normal human lung. Hyperoxia has no significant effect on vascular resistance in the normal human lung.
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