Literature DB >> 8272584

Local pulmonary blood flow: control and gas exchange.

D W Sheehan1, L E Farhi.   

Abstract

We studied the local response of the pulmonary vasculature to combined changes in alveolar PO2 and PCO2 in the right apical lobe (RAL) of six conscious sheep. That lobe inspired an O2-CO2-N2 mixture adjusted to produce one of 12 alveolar gas compositions: end-tidal PCO2 (PETCO2) of 40, 50, and 60 Torr, each coupled with end-tidal PO2 (PETO2) of 100, 75, 50, and 25 Torr. In addition, at each of the four PETO2, the inspired CO2 was set to 0 and PETCO2 was allowed to vary as RAL perfusion changed. The remainder of the lung, which served as control (CL) inspired air. Fraction of the total pulmonary blood flow going to the RAL (%QRAL) was obtained by comparing the methane elimination from the RAL to that of the whole lung, and expressed as a percentage of that fraction at PETCO2 = 40, PETO2 = 100. Cardiac output, pulmonary vascular pressures, and CL gas tensions were unaffected or only minimally affected by changes in RAL gas composition. A drop in PO2 from 100 to 50 Torr decreased local blood flow by 60% in normocapnia and by 66% at a PCO2 of 60. At all levels of oxygenation, an increase in PCO2 from 40 to 60 reduced QRAL by nearly 50%. With these stimulus-response data, we developed a model of gas exchange, which takes into account the effects of test segment size on blood flow diversion. This model predicts that: (1) when the ventilation to one compartment of a two compartment lung is progressively decreased, PAO2 remains above 60 Torr for up to 60% reductions in alveolar ventilation, irrespective of compartment size; (2) the decrease in PAO2 that occurs at altitude is accompanied by a drop in PACO2 that limits the decrease in conductance and minimizes the pulmonary hypertension; and (3) as we stand, local blood flow control by the alveolar gas tensions halves the alveolar-arterial PO2 and PCO2 differences imposed by gravity.

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Year:  1993        PMID: 8272584     DOI: 10.1016/0034-5687(93)90059-j

Source DB:  PubMed          Journal:  Respir Physiol        ISSN: 0034-5687


  6 in total

1.  Reply to Dorrington et al. and to Swenson: "Hypercapnic Pulmonary Vasoconstriction Contributes to Regional Perfusion Distribution: Relevance to Asthma" and "Hypercapnic Pulmonary Vasoconstriction as a Mechanism for Regional Perfusion Redistribution in Asthma".

Authors:  Vanessa J Kelly; Tilo Winkler; R Scott Harris
Journal:  Am J Respir Crit Care Med       Date:  2018-03-01       Impact factor: 21.405

2.  Regional pulmonary perfusion patterns in humans are not significantly altered by inspiratory hypercapnia.

Authors:  Amran K Asadi; Rui Carlos Sá; Tatsuya J Arai; Rebecca J Theilmann; Susan R Hopkins; Richard B Buxton; G Kim Prisk
Journal:  J Appl Physiol (1985)       Date:  2019-06-06

Review 3.  Human pulmonary vascular responses to hypoxia and hypercapnia.

Authors:  K L Dorrington; N P Talbot
Journal:  Pflugers Arch       Date:  2004-10       Impact factor: 3.657

4.  Extent to which pulmonary vascular responses to PCO2 and PO2 play a functional role within the healthy human lung.

Authors:  Keith L Dorrington; George M Balanos; Nick P Talbot; Peter A Robbins
Journal:  J Appl Physiol (1985)       Date:  2010-02-25

Review 5.  Hypoxic pulmonary vasoconstriction.

Authors:  J T Sylvester; Larissa A Shimoda; Philip I Aaronson; Jeremy P T Ward
Journal:  Physiol Rev       Date:  2012-01       Impact factor: 46.500

6.  Variations in alveolar partial pressure for carbon dioxide and oxygen have additive not synergistic acute effects on human pulmonary vasoconstriction.

Authors:  Quentin P P Croft; Federico Formenti; Nick P Talbot; Daniel Lunn; Peter A Robbins; Keith L Dorrington
Journal:  PLoS One       Date:  2013-07-31       Impact factor: 3.240

  6 in total

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