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R L Capen

Publications and source records attributed to R L Capen.

22 records · Page 2Linked to original sources

Diffusing capacity of the lung during hypoxia: role of capillary recruitment.

We have used in vivo microscopy to show that airway hypoxia caused pulmonary capillary recruitment. To determine whether the recruited capillaries add to the surface area for gas exchange, we measured the diffusing capacity of the lung for carbon monoxide before and after inducing recruitment with hypoxia. Diffusing capacity increased during hypoxia. However, some increase in diffusing capacity was expected, since there were fewer oxygen molecules to compete with carbon monoxide for hemoglobin-binding sites. To determine the effect of capillary recruitment alone on diffusing capacity, we held hypoxia constant while infusing a vasodilator to diminish recruitment. Diffusing capacity decreased concomitantly as recruitment diminished. These results indicate that our microscopic observations reflect a widespread recruitment that increases the gas exchange surface area.

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Capillary recruitment during airway hypoxia: role of pulmonary artery pressure.

Hypoxia has been shown to cause an increased number of pulmonary capillaries to be perfused. Changes in cardiac output and left atrial pressure have been previously ruled out as causes of this capillary recruitment. Increased pulmonary vein pressure and increased pulmonary artery pressure remain as two potential mechanisms. To differentiate between these two possible causes, we measured pulmonary artery and vein pressures with directly placed catheters and capillary recruitment with in vivo microscopy. During isocapnic hypoxia pulmonary artery pressure doubled, observed capillary recruitment increased fivefold, and pulmonary vein pressure remained constant. When the vasodilator prostaglandin E1 was infused during hypoxia, pulmonary artery pressure and capillary recruitment fell to control values and pulmonary vein pressure remained constant. Since capillary recruitment correlated with pulmonary artery pressure in each dog, but not with pulmonary vein pressure, we conclude that arterial, not venous, constriction is the probable cause of this recruitment.

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