PULMONARY-ARTERY OCCLUSION AND LUNG COLLAPSE DEPLETES RABBIT LUNG ADENOSINE-TRIPHOSPHATE

Background: Although the bronchial circulation has traditionally been thought to provide adequate blood flow for the lung when the pulmonary artery is obstructed, recent studies have demonstrated that pulmonary artery occlusion results in lung injury. We hypothesized that after p ulmonary artery occlusion, aerobic lung metabolic function is altered. We studied the changes in the concentration of adenine nucleotides as markers of injury in the intact rabbit lung after pulmonary artery oc clusion in the presence and absence of pneumothorax. Methods: A thorac otomy was performed on the rabbits, and an occlusive microvascular cla mp was placed on the left pulmonary artery. The rabbit lungs were stud ied after 24 h of in vivo left pulmonary artery occlusion (n = 5), 24 h of left pulmonary artery occlusion with the lung collapsed by pneumo thorax (n = 6), or 24 h of lung collapse alone (n = 5). Results: Adeno sine triphosphate concentrations of the occluded left lung decreased d ramatically at 24 h in the group with pulmonary artery occlusion and c ollapse (adenosine triphosphate concentration 196 +/- 32 ng/g for the left lung and 1,479 +/- 197 ng/g for the right lung; P < 0.001). There were no differences between the lungs in the rabbits undergoing occlu sion alone or collapse alone. Conclusions: After pulmonary artery occl usion or lung collapse, adenine nucleotides are preserved if ventilati on is continued. The increased permeability of rabbit lungs after 24 h of left pulmonary artery occlusion alone cannot be explained on the b asis of depletion of high-energy phosphates. In the absence of ventila tion due to lung collapse, pulmonary artery occlusion results in decre ased adenosine triphosphate concentrations, demonstrating that the res idual circulations (bronchial and pulmonary venous flow) are inadequat e to support normal tung aerobic metabolism.