Effect of wood combustion smoke inhalation on angiotensin-1-converting enzyme in the dog.
One lung of each dog was exposed to smoke from burning pine wood, while the other was subjected to acute hypoxia. Angiotensin-1-converting enzyme (ACE) activity in biopsied tissue of the smoke-exposed lung was markedly increased immediately after the injury and even higher 30 minutes later. No change in ACE activity was observed in the hypoxic contralateral lung. Serum ACE activity did not change significantly following anesthesia and before smoke inhalation. Serum aldosterone and cortisol levels increased at this juncture. Smoke inhalation caused intra-alveolar hemorrhages and edema. Pulmonary and systolic, diastolic and mean pressures, pulmonary capillary, wedge pressure, cardiac output and systemic and pulmonary arteriolar resistances remained unchanged throughout the experiment. The changes of ACE activity are presumably a direct effect of smoke inhalation. They are seen as an early response of the lung endothelial cells to many types of injury (chronic hypoxia, bleomycin or monocrotaline administration) and may represent an important step in the development of the organ's response to the injury.
D000450:Aldosterone / Q000097:blood; D000818:Animals; D004285:Dogs; D004789:Enzyme Activation; D006854:Hydrocortisone / Q000097:blood; D000860:Hypoxia / Q000201:enzymology*; D008168:Lung / Q000201:enzymology* / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism; D012906:Smoke / Q000009:adverse effects*; D014934:Wood
D011506:Proteins; D012906:Smoke; D000450:Aldosterone; D007703:Peptidyl-Dipeptidase A; D006854:Hydrocortisone