Lung enzymes in emphysematous rats: effects of progestagens, antiphlogistics and metabolic inhibitors.
Chronic exposure of rats to 10% aerosols of papain or trypsin resulted in marked increases in lung weights and lung beta-glucuronidase and arylsulfatase activities. Destruction of alveolar walls was demonstrated microscopically as a decrease in the number of air spaces touching a line of known length. The pregnenes, progesterone and medroxyprogesterone acetate, but not the 19-nortestosterone derivative norethindrone, partially prevented the papain-induced breakdown of alveolar septa and elevation of beta-glucuronidase. The steroidal anti-inflammatory agent, paramethasone, completely inhibited the rise in lung weight and beta-glucuronidase activity, but did not prevent destruction of alveolar walls. The non-steroidal anti-inflammatory agent, indomethacin, afforded little or no protection. Limited prophylaxis against both histological and enzymatic changes was observed in rats treated with the anti-metabolite, cyclophosphamide, and the proteolytic enzyme inhibitor, aprotinin. The various lung abnormalities resulting from papain inhalation may thus be individually influenced by specific pharmacologic agents.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000963:Antimetabolites / Q000494:pharmacology*; D001192:Arylsulfatases / Q000378:metabolism; D005966:Glucuronidase / Q000378:metabolism; D008168:Lung / Q000201:enzymology*; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010206:Papain; D011372:Progestins / Q000494:pharmacology*; D011650:Pulmonary Alveoli / Q000187:drug effects; D011656:Pulmonary Emphysema / Q000139:chemically induced / Q000201:enzymology*; D051381:Rats; D013997:Time Factors; D014357:Trypsin
D000893:Anti-Inflammatory Agents; D000963:Antimetabolites; D011372:Progestins; D001192:Arylsulfatases; D005966:Glucuronidase; D014357:Trypsin; D010206:Papain