sodium-morrhuate and Hypertension--Pulmonary

Sodium morrhuate and sodium tetradecylsulfate are injected during endoscopic sclerotherapy to control variceal bleeding. When administered to sheep they cause transient pulmonary hypertension and increase protein poor lung lymph flow. To determine the etiology of these alterations, we studied three groups of sheep after establishing acute lung lymph fistulas. In Group 1, indomethacin or ibuprofen was infused. In Group 2, 2.5 cc of sodium morrhuate was injected alone (2A) or after indomethacin or ibuprofen pretreatment (2B). In Group 3, 2.5 cc of sodium tetradecylsulfate was given intravenously either alone (3A) or after indomethacin or ibuprofen (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 sodium morrhuate and from 1.2 +/- .62 to 2.7 +/- 1.7 cc/30 mins at 30 minutes after sodium tetradecylsulfate and the lymph/plasma albumin ratio fell. Increased lymph flow persisted through 120 minutes. In those animals receiving a sclerosing agent after indomethacin or ibuprofen (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 pulmonary hypertension and increased protein poor lymph flow are mediated by prostaglandins.

Topics: Animals; Blood Pressure; Cyclooxygenase Inhibitors; Drug Combinations; Female; Hypertension, Pulmonary; Ibuprofen; Indomethacin; Lung; Lymph; Lymphatic Diseases; Organ Size; Pulmonary Wedge Pressure; Sclerosing Solutions; Serum Albumin; Sheep; Sodium Morrhuate; Sodium Tetradecyl Sulfate

Topics: Animals; Esophageal and Gastric Varices; Fatty Acids; Humans; Hypertension, Pulmonary; Sclerosing Solutions; Sheep; Sodium Morrhuate

Two of 30 patients with esophageal varices had respiratory distress develop within 8-24 h of esophageal sclerotherapy. Evidence of aspiration and sepsis were absent in these two patients with the clinical picture of adult respiratory distress syndrome. To investigate the possible etiologic role of sodium morrhuate in this syndrome, a sheep model was established and pulmonary hemodynamics, lung lymph flow, and albumin concentration were measured before and after the intravenous injection of 2.5-15.0 cm3 of sodium morrhuate. In all 8 animals studied, mean pulmonary artery pressures increased from 11.6 +/- 2.8 to 32.8 +/- 4.9 mmHg (p less than 0.01) 30 s after injection. These pressures returned to baseline values over 120 min. Lymph flow increased from 0.91 +/- 0.89 to 2.8 +/- 1.5 ml/30 min at 90 min postinjection (p less than 0.05) and returned to baseline values in animals monitored for 6-8 h. The lymph/plasma albumin ratio decreased from 0.856 +/- 0.08 to 0.74 +/- 0.01 (p less than 0.05) 120 min postinjection. Pulmonary edema was not evident histologically or gravimetrically (wet/dry weight ratio was 3.65 +/- 0.3 and not different from normal). It was concluded that sodium morrhuate injection in sheep causes marked but transient pulmonary hypertension associated with an increased lymph flow of relatively protein-poor lymph. Sodium morrhuate esophageal sclerotherapy may affect pulmonary hemodynamics and contribute to respiratory difficulties in patients.

Topics: Animals; Esophageal and Gastric Varices; Fatty Acids; Female; Gastrointestinal Hemorrhage; Humans; Hypertension, Pulmonary; Lymph; Male; Middle Aged; Pulmonary Circulation; Pulmonary Wedge Pressure; Respiratory Distress Syndrome; Sclerosing Solutions; Serum Albumin; Sheep; Sodium Morrhuate