The XXXX of sclerosing agents is prevented by cyclooxygenase inhibitors.

@entity742 @entity548 @entity13420 @entity5018 @entity120 @entity2918 @entity8191 @entity3352
@entity8191 and @entity13420 are injected during endoscopic sclerotherapy to control variceal @entity548 . When administered to @entity742 they cause transient @entity120 and increase protein poor lung lymph flow. To determine the etiology of these alterations, we studied three groups of @entity742 after establishing acute lung lymph fistulas. In Group 1, @entity3352 or @entity5018 was infused. In Group 2, 2.5 cc of @entity8191 was injected alone (2A) or after @entity3352 or @entity5018 pretreatment (2B). In Group 3, 2.5 cc of @entity13420 was given intravenously either alone (3A) or after @entity3352 or @entity5018 (3B). When sclerosing agents were given alone (Group 2A and 3A) pulmonary artery pressures increased three-fold at 30 seconds postinjection to 37 +/- 4.4 and 39 +/- 5.7 mmHg respectively with a slow return to baseline over two hours. Lymph flow increased significantly from 1.3 +/- 1.5 to 2.7 +/- 1.5 cc/30 minutes after @entity8191 and from 1.2 +/- .62 to 2.7 +/- 1.7 cc/30 mins at 30 minutes after @entity13420 and the lymph/plasma albumin ratio fell. Increased lymph flow persisted through 120 minutes. In those animals receiving a sclerosing agent after @entity3352 or @entity5018 (2B and 3B) there was no change in pulmonary artery pressure, lymph flow, lymph plasma albumin ratio, or lung wet weight to dry weight ratios. We conclude that the @entity120 and increased protein poor lymph flow are mediated by @entity2918 .
