Evidence for a functional link between stress response and vascular control in hepatic portal circulation.
Am J Physiol
; 271(5 Pt 1): G929-35, 1996 Nov.
Article
de En
| MEDLINE
| ID: mdl-8944709
ABSTRACT
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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Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Système porte
/
Choc hémorragique
/
Transcription génétique
/
Heme oxygenase (decyclizing)
/
Foie
Limites:
Animals
Langue:
En
Journal:
Am J Physiol
Année:
1996
Type de document:
Article
Pays d'affiliation:
Allemagne