Lymph Circulation in Hepatic Cirrhosis: Effect of Portacaval Shunt
- MARLYS HEARST WITTE, M.D.;
- ALLAN E. DUMONT, M.D.;
- WILLIAM R. COLE, M.D.;
- CHARLES L. WITTE, M.D.; and
- KATHLEEN KINTNER, A.B.
- Requests for reprints should be addressed to Marlys Hearst Witte, M.D., Unit 1 (Washington University) Surgery, St. Louis City Hospital, 1515 Lafayette Ave., St. Louis, Mo. 63104
SUMMARY
To determine the relative contribution of the liver and extrahepatic portal bed to increased flow of thoracic duct lymph in hepatic cirrhosis, thoracic duct lymph was examined in 84 patients with nutritional or post-necrotic cirrhosis, including 11 after portosystemic shunt. Lymph flow, pressure, protein content, and sulfobromophthalein (BSP) retention at 45 min were measured. Total protein content of lymph from liver and small intestine was determined in nine patients at laparotomy and was compared with plasma, thoracic duct lymph, and ascitic fluid. Thoracic duct lymph studies were repeated after portacaval shunt in seven patients.
The observations indicate that when post-sinusoidal obstruction predominates highly permeable liver sinusoids are the major source of increased thoracic duct lymph high in protein and BSP; but, as presinusoidal block develops, liver lymph is diluted in the thoracic duct by increasing amounts of low-protein intestinal lymph poor in BSP, and thoracic duct lymph protein and BSP fall. After extrahepatic portal hypertension is relieved by a portacaval shunt, thoracic duct lymph flow decreases while protein and BSP content rise. The shunt eliminates excess capillary filtrate from the extrahepatic portal bed and probably also reduces excess capillary filtrate from the liver.
Article and Author Information
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From the Departments of Medicine and Surgery, Washington University School of Medicine, St. Louis, Mo.; and New York University School of Medicine, New York, N. Y.
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Supported in part by grants HE-09073, HE-11904, HE-11034, and AM-10875, U. S. Public Health Service, Washington, D. C.; Institute of Medical Education and Rehabilitation of St. Louis City Hospital, St. Louis, Mo.; Licensed Beverage Industries, Inc., New York, N. Y.; American Heart Association, New York, N. Y.; and the John A. Hartford Foundation, Inc., New York, N. Y. Part of the research was conducted on the U. S. Public Health Service-supported clinical research units at Barnes Hospital, St. Louis, Mo., and Bellevue Hospital, New York, N. Y.
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- Received July 8, 1968.
- Accepted October 29, 1968.
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