AJP - Gastrointestinal and Liver Physiology, Vol 271, Issue 5 929-G935, Copyright © 1996 by American Physiological Society

ARTICLES

Evidence for a functional link between stress response and vascular control in hepatic portal circulation

M. Bauer, B. H. Pannen, I. Bauer, C. Herzog, G. A. Wanner, R. Hanselmann, J. X. Zhang, M. G. Clemens and R. Larsen
Department of Anesthesiology and Critical Care Medicine, University of the Saarland, Homburg, Germany.

Heme oxygenase (HO)-derived carbon monoxide (CO) may contribute to vascular control through elevation of guanosine 3',5'-cyclic monophosphate. In the present study, we investigated the functional significance of expression of the isoenzyme HO-1 (heat-shock protein 32) in liver after hemorrhage/resuscitation (H/R) in rats anesthetized with pentobarbital sodium. An increase of mRNA levels for HO-1 was observed at 3 h after resuscitation, followed by induction of the protein at 6 h in pericentral hepatocytes and sinusoidal lining cells. Concomitantly, lower portal resistance was observed in H/R (0.33 +/- 0.060 mmHg.ml-1.min) compared with control rats (0.47 +/- 0.035 mmHg.ml-1.min). Blockade of the HO-CO pathway by tin protoporphyrin-IX (SnPP-IX) led to a transient increase in portal pressure with no effect on portal low in controls, whereas an increase in pressure and a decrease in flow contributed to the sustained increase in portal resistance after H/R. These results indicate that HO contributes to maintenance of hepatic perfusion in vivo under stressful conditions, suggesting a functional link between stress response and vascular control in portal circulation.

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