Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension

J. V. Sitzmann, G. B. Bulkley, M. C. Mitchell, K. Campbell

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

To determine the possible role of prostacyclin (PGI2) as a mediator of the splanchnic hyperemia seen with portal hypertension, the portal and mesenteric hemodynamics in normal and portal hypertensive rabbits were studied before and after cyclo-oxygenase blockade. Three weeks after partial portal vein ligation, splenic pulp pressure was elevated from 4.3 ± 0.9 to 9.8 ± 0.8 mmHg (p < 0.01). Mesenteric blood flow increased from 77.0 ± 4.7 ml · min-1 · 100 g-1 to 99.1 ± 5.19 ml/min-1/100 g-1. Mesenteric vascular resistance fell from 0.82 ± 0.6 mmHg/ml-1/min-1 to 0.49 ± 0.07 mmHg/ml-1/min-1 (p < 0.01). These hemodynamic changes were associated with a 27.3 ± 0.2% rise in systemic arterial levels of PGI2 (p < 0.01) and were substantially ameliorated by cyclo-oxygenase blockade with indomethacin. The effects of indomethacin blockade were reserved by exogenous PGI2. Moreover, in normotensive rabbits, infusion of PGI2 reproduced the splanchnic hyperemia and caused a very small but significant increase in portosystemic shunting. These findings support the previously proposed concept that splanchnic hyperemia may contribute to the maintenance of chronic portal hypertension. Furthermore, they suggest that this effect may be partially mediated by splanchnic PGI2 production.

Original languageEnglish (US)
Pages (from-to)322-327
Number of pages6
JournalAnnals of Surgery
Volume209
Issue number3
StatePublished - 1989

Fingerprint

Viscera
Hyperemia
Portal Hypertension
Epoprostenol
Prostaglandin-Endoperoxide Synthases
Indomethacin
Hemodynamics
Rabbits
Portal Vein
Vascular Resistance
Ligation
Maintenance
Pressure

ASJC Scopus subject areas

  • Surgery

Cite this

Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension. / Sitzmann, J. V.; Bulkley, G. B.; Mitchell, M. C.; Campbell, K.

In: Annals of Surgery, Vol. 209, No. 3, 1989, p. 322-327.

Research output: Contribution to journalArticle

Sitzmann, JV, Bulkley, GB, Mitchell, MC & Campbell, K 1989, 'Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension', Annals of Surgery, vol. 209, no. 3, pp. 322-327.
Sitzmann, J. V. ; Bulkley, G. B. ; Mitchell, M. C. ; Campbell, K. / Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension. In: Annals of Surgery. 1989 ; Vol. 209, No. 3. pp. 322-327.
@article{cdd70d8000444095a731f183d57fbd17,
title = "Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension",
abstract = "To determine the possible role of prostacyclin (PGI2) as a mediator of the splanchnic hyperemia seen with portal hypertension, the portal and mesenteric hemodynamics in normal and portal hypertensive rabbits were studied before and after cyclo-oxygenase blockade. Three weeks after partial portal vein ligation, splenic pulp pressure was elevated from 4.3 ± 0.9 to 9.8 ± 0.8 mmHg (p < 0.01). Mesenteric blood flow increased from 77.0 ± 4.7 ml · min-1 · 100 g-1 to 99.1 ± 5.19 ml/min-1/100 g-1. Mesenteric vascular resistance fell from 0.82 ± 0.6 mmHg/ml-1/min-1 to 0.49 ± 0.07 mmHg/ml-1/min-1 (p < 0.01). These hemodynamic changes were associated with a 27.3 ± 0.2{\%} rise in systemic arterial levels of PGI2 (p < 0.01) and were substantially ameliorated by cyclo-oxygenase blockade with indomethacin. The effects of indomethacin blockade were reserved by exogenous PGI2. Moreover, in normotensive rabbits, infusion of PGI2 reproduced the splanchnic hyperemia and caused a very small but significant increase in portosystemic shunting. These findings support the previously proposed concept that splanchnic hyperemia may contribute to the maintenance of chronic portal hypertension. Furthermore, they suggest that this effect may be partially mediated by splanchnic PGI2 production.",
author = "Sitzmann, {J. V.} and Bulkley, {G. B.} and Mitchell, {M. C.} and K. Campbell",
year = "1989",
language = "English (US)",
volume = "209",
pages = "322--327",
journal = "Annals of Surgery",
issn = "0003-4932",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Role of prostacyclin in the splanchnic hyperemia contributing to portal hypertension

AU - Sitzmann, J. V.

AU - Bulkley, G. B.

AU - Mitchell, M. C.

AU - Campbell, K.

PY - 1989

Y1 - 1989

N2 - To determine the possible role of prostacyclin (PGI2) as a mediator of the splanchnic hyperemia seen with portal hypertension, the portal and mesenteric hemodynamics in normal and portal hypertensive rabbits were studied before and after cyclo-oxygenase blockade. Three weeks after partial portal vein ligation, splenic pulp pressure was elevated from 4.3 ± 0.9 to 9.8 ± 0.8 mmHg (p < 0.01). Mesenteric blood flow increased from 77.0 ± 4.7 ml · min-1 · 100 g-1 to 99.1 ± 5.19 ml/min-1/100 g-1. Mesenteric vascular resistance fell from 0.82 ± 0.6 mmHg/ml-1/min-1 to 0.49 ± 0.07 mmHg/ml-1/min-1 (p < 0.01). These hemodynamic changes were associated with a 27.3 ± 0.2% rise in systemic arterial levels of PGI2 (p < 0.01) and were substantially ameliorated by cyclo-oxygenase blockade with indomethacin. The effects of indomethacin blockade were reserved by exogenous PGI2. Moreover, in normotensive rabbits, infusion of PGI2 reproduced the splanchnic hyperemia and caused a very small but significant increase in portosystemic shunting. These findings support the previously proposed concept that splanchnic hyperemia may contribute to the maintenance of chronic portal hypertension. Furthermore, they suggest that this effect may be partially mediated by splanchnic PGI2 production.

AB - To determine the possible role of prostacyclin (PGI2) as a mediator of the splanchnic hyperemia seen with portal hypertension, the portal and mesenteric hemodynamics in normal and portal hypertensive rabbits were studied before and after cyclo-oxygenase blockade. Three weeks after partial portal vein ligation, splenic pulp pressure was elevated from 4.3 ± 0.9 to 9.8 ± 0.8 mmHg (p < 0.01). Mesenteric blood flow increased from 77.0 ± 4.7 ml · min-1 · 100 g-1 to 99.1 ± 5.19 ml/min-1/100 g-1. Mesenteric vascular resistance fell from 0.82 ± 0.6 mmHg/ml-1/min-1 to 0.49 ± 0.07 mmHg/ml-1/min-1 (p < 0.01). These hemodynamic changes were associated with a 27.3 ± 0.2% rise in systemic arterial levels of PGI2 (p < 0.01) and were substantially ameliorated by cyclo-oxygenase blockade with indomethacin. The effects of indomethacin blockade were reserved by exogenous PGI2. Moreover, in normotensive rabbits, infusion of PGI2 reproduced the splanchnic hyperemia and caused a very small but significant increase in portosystemic shunting. These findings support the previously proposed concept that splanchnic hyperemia may contribute to the maintenance of chronic portal hypertension. Furthermore, they suggest that this effect may be partially mediated by splanchnic PGI2 production.

UR - http://www.scopus.com/inward/record.url?scp=0024523451&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024523451&partnerID=8YFLogxK

M3 - Article

VL - 209

SP - 322

EP - 327

JO - Annals of Surgery

JF - Annals of Surgery

SN - 0003-4932

IS - 3

ER -