Responses of serum and lung angiotensin-converting enzyme activities in the early phase of pulmonary damage induced by oleic acid in dogs.

Changes in angiotensin-converting enzyme (ACE) activity in the lung tissue, edema fluid, and bloodstream were studied during induction of lung edema by oleic acid. Left lungs of 25 mongrel dogs were unilaterally treated with oleic acid (0.1 ml/kg) injected into the right atrium during right pulmonary artery occlusion for 2.5 min. Lung tissue and serum ACE activities and physiologic parameters were followed for as long as 180 min. Serum ACE activity increased to 106% at 2.5 min (p less than 0.025) and to 128% at 180 min. The ACE activity of treated lung tissue decreased compared with the zero time control in terms of tissue DNA content (at 180 min, p less than 0.05). Furthermore, the left to right activity ratio of the precipitate fraction decreased to 0.59 as early as 5 min after oleic acid injection (p less than 0.01). Changes in these ACE activities preceded those of arterial oxygen tension and base transthoracic electrical impedance. Edema fluid at 45 min had a specific activity that was 1.62 times greater than that in serum. These data indicated that the change in ACE activity reflected the impairment of pulmonary vascular endothelial cells and that the oleic acid injured endothelial cells of the pulmonary capillaries as early as 2.5 min after administration.