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Am J Physiol Gastrointest Liver Physiol 270: G6-G13, 1996;
0193-1857/96 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 270, Issue 1 6-13, Copyright © 1996 by American Physiological Society

ARTICLES

Hepatic involvement in pancreatitis-induced lung damage

D. Closa, M. Bardaji, G. Hotter, N. Prats, E. Gelpi, L. Fernandez-Cruz and J. Rosello-Catafau
Department of Medical Bioanalysis, Centro de Investigacion y Desarrollo, Consejo Superior de Investigaciones Cientificas, Barcelona, Spain.

The role of liver in the respiratory dysfunction associated with acute pancreatitis has been evaluated. For this purpose, an experimental necrohemorrhagic pancreatitis was induced in rats by intraductal administration of 3.5% sodium taurocholate. Additionally, a portocaval shunt was performed before induction of acute pancreatitis to prevent the initial passage through the liver of substances released by the pancreas. Twelve hours after the induction of pancreatitis, increases in lung prostacyclin and thromboxane B2 synthesis, decreased lung superoxide dismutase activity, and increases in plasma phospholipase A2 activity were found. In addition, inflammatory injury was evidenced in lung by histopathological analysis. The portocaval shunt was able to prevent the metabolic changes and ameliorate the inflammatory process in the lung, suggesting that the liver plays an active role in the systemic inflammatory response to acute pancreatitis.


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S Furue, Y Hori, K Kuwabara, J Ikeuchi, H Onoyama, M Yamamoto, and K Tanaka
Increased activity of group II phospholipase A2 in plasma in rat sodium deoxycholate induced acute pancreatitis
Gut, December 1, 1997; 41(6): 826 - 831.
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