Pulmonary parenchymal damage often occurs after airway injury. Bronchial venous drainage empties into the pulmonary microvasculature. We developed an in vivo model to study the bronchopulmonary portal system after smoke inhalation injury. Eight ewes were instrumented with hydraulic occluders on the left pulmonary artery (LPA), the left pulmonary vein, and the bronchoesophageal artery (BEA); a catheter in the LPA; and Swan-Ganz and femoral artery catheters. The vasculature between the occluders was defined as pouch. At stable mean arterial and right pulmonary arterial pressures, LPA occlusion reduced the left pulmonary artery pressure (LPAP) from 17 ±1 mmHg to 8 ± 1 mmHg (p < .05). After left pulmonary vein occlusion, LPAP rose to 28 ± 4 mmHg (p < .05 vs. baseline), indicating that systemic blood had entered the pouch. Opening the pouch to atmospheric pressure revealed an anastomotic bronchial blood flow (anastomotic Qbr) of .76 ±.11 % of cardiac output (CO). BEA occlusion reduced the anastomotic Qbr to .32 ± .06% of CO (p < .05). Smoke inhalation injury resulted in a further increase in the maximal 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 reduced to .40 ± .09% of CO (p < .05) by BEA occlusion. Inhalation injury increased the anastomotic Qbr mainly due to BEA vasodilatation. Because the BEA supplies the injured airway, it may deliver deleterious material to the lung parenchyma.
ASJC Scopus subject areas
- Emergency Medicine
- Critical Care and Intensive Care Medicine