Evidence for a functional link between stress response and vascular
control in hepatic portal circulation.
Bauer, Michael, Benedikt H. J. Pannen, Inge Bauer, Carsten Herzog,
Guido A. Wanner, Rainer Hanselmann, Jian X. Zhang, Mark G. Clemens,
and Reinhard Larsen.
Depts. of Anesthesiology and Critical Care Medicine, Experimental,
and Trauma Surgery, University of the Saarland, Dept. of
Anesthesiology, Albert-Ludwig-University, Freiburg, F.R.G., and Dept.
of Surgery, Johns Hopkins University, Baltimore, MD, U.S.A.
APStracts 3:0159G, 1996.
Heme oxygenase (HO) derived carbon monoxide (CO) may contribute to
vascular control through elevation of cyclic 3':5' guanosine
monophosphate. In the present study we investigated functional
significance of expression of the isoenzyme HO-1 (heat shock protein
32) in liver following hemorrhage / resuscitation (H/R) in
pentobarbital anesthetized rats. An increase of mRNA levels for HO-1
was observed at three hours after resuscitation followed by induction
of the protein at 6h in pericentral hepatocytes and sinusoidal lining
cells. Concomitantly, lower portal resistance was observed in H/R
(0.33 +/- 0.060 mmHg*min*ml-1) as compared to control (0.47 +/- 0.035
mmHg*min*ml-1). Blockade of HO/CO pathway by tin protoporphyrin-IX
(SnPP-IX) led to a transient increase in portal pressure with no
effect on portal flow in controls, while 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.
Received 16 April 1996; accepted in final form 8 August 1996.
APS Manuscript Number G140-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996