INHALATION INJURY INCREASES THE ANASTOMOTIC BRONCHIAL BLOOD-FLOW IN THE POUCH MODEL OF THE LEFT OVINE LUNG

Pulmonary parenchymal damage often occurs after airway injury. Bronchi al venous drainage empties into the pulmonary microvasculature. We dev eloped an in vivo model to study the bronchopulmonary portal system af ter smoke inhalation injury. Eight ewes were instrumented with hydraul ic occluders on the left pulmonary artery (LPA), the left pulmonary ve in, and the bronchoesophageal artery (BEA); a catheter in the LPA; and Swan-Ganz and femoral artery catheters. The vasculature between the o ccluders was defined as pouch. At stable mean arterial and right pulmo nary arterial pressures, LPA occlusion reduced the left pulmonary arte ry pressure (LPAP) from 17 +/- 1 mmHg tb 8 +/- 1 mmHg (p <.05). After left pulmonary vein occlusion, LPAP rose to 28 +/- 4 mmHg (p <.05 vs. baseline), indicating that systemic brood had entered the pouch. Openi ng the pouch to atmospheric pressure revealed an anastomotic bronchial blood flow (anastomotic Qbr) of .76 +/- .11% af cardiac output (GO). BEA occlusion reduced the anastomotic Qbr to .32 +/- .06% of CO (p <.0 5). Smoke inhalation injury resulted in a further increase in the maxi mal LPAP to 38 +/- 5 mmHg (p <.05 vs. right pulmonary artery pressure) . The anastomotic Qbr rose to 1.29 +/- .13% of CO (p <.05) and was red uced to .40 +/- .09% of CD (p <.05) by BEA occlusion. Inhalation injur y increased the anastomotic Qbr mainly due to BEA vasodilatation. Beca use the BEA supplies the injured airway, it may deliver deleterious ma terial to the lung parenchyma.