Effect of acute smoke inhalation on angiotensin converting enzyme, plasminogen activator, and angiotensin-II in the dog.

Smoke inhalation injuries in humans are associated with many uncontrolled variables which impact on the lung and make the cause of the pulmonary response difficult to assess. In this report, an established model of smoke inhalation injury in the dog was used to study the early responses of tissue and serum angiotensin-converting enzyme (ACE), tissue plasminogen activator (PLA), and plasma angiotensin II. Animals were exposed to smoke from burning sawdust and kerosene for five minutes. The hemodynamic and pulmonary mechanical responses were typical with a rise in pulmonary artery pressure, pulmonary vascular resistance, and venous admixture (shunt fraction) while dynamic compliance fell. Within five minutes of smoke exposure, lung ACE declined without any change in serum ACE. Lung PLA dropped one hour after injury. Plasma angiotensin II increased within 30 minutes without evidence for systemic hypertension. These early enzymatic changes substantiate the presence of pulmonary endothelial damage known to occur in this form of chemical injury. These changes may condition the lung's physiologic response to the injury and to additional stresses which are multiple when smoke inhalation occurs in conjunction with a cutaneous burn.