Small airways impairment during progressive hemorrhage and early shock in dogs

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Abstract
As hemorrhagic shock induces an increase of long capillary permeability in dogs, fluid flow into the interstitial tissue should 1st disturb small airways mechanics. Prone dogs were submitted to constant arterial hemorrhage until blood pressure fell below 50 Torr (shock). During hemorrhage, closing volume (133Xe bolus) (CV/VC) increased significantly (preshock period). During shock CV/VC came back to control values (shock period), but increased again during prolonged shock. Lung volumes, static pressure-volume curves, maximal expiratory flows in air, and total lung and upstream resistances were not affected in the two 1st periods. Maximal expiratory flow after 80% He-20% O2 breathing decreased during hemorrhage, but returned to control during shock. Bilateral vagotomy alone or followed by isoproterenol did not abolish the increase of CV/VC. Changes in airway mechanics due to arterial hemorrhage prior to the state of fully developed shock were shown. These abnormalities are not explained by changes in bronchomotor tone or alterations in the elastic properties of the lung but are probably due to peribronchiolar edema. The drop of pulmonary artery pressure in shock could account for a short functional improvement.

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