Prostacyclin production in acute, chronic, and long-term experimental portal hypertension
Sitzmann, J.V.; Campbell, K.; Wu, Y.; St Clair, C.
Surgery 115(3): 290-294
1994
ISSN/ISBN: 0039-6060 PMID: 8128353 Document Number: 433901
Background. Chronic portal hypertension (PHT) is characterized by a high portosystemic shunt (PSS) and increased splanchnic bloodflow. It has been suggested that the splanchnic vasodilator, prostacyclin (PGI-2), mediates this increased flow. We studied splanchnic PGI-2 production both in normal rabbits and in three groups of rabbits after Partial portal vein ligation (PVL-PHT): acute (within 30 minutes of ligation), chronic (3 weeks after ligation), and long-term (3 months after ligation) to determine whether increased splanchnic production is a mechanism for the elevated PGI-2 in PHT. Methods. Levels of 6-keto prostaglandin F-1alpha were determined by radioimmunoassay, and splanchnic hemodynamics were measured with Doppler flowmetry in four groups of rabbits: portal normotensive rabbits, and PVL-PHT rabbits 30 minutes, 3 weeks, or 3 months after partial PVL. Splanchnic PGI-2 production (PGI-2 PROD) was then calculated. Results. Portal pressure and PSS in chronic and long-term groups were significantly elevated in all groups compared with normals (p lt 0.001). Splanchnic bloodflow initially fell from 84 +- 4.8 to 37.4 +- 7 m 1/min/ 7 00 gm immediately and then rose to 144.7 +- 9.6 ml/min/100 gm and 137 +- 15 ml/min/100 gm at 3 weeks and 3 months after ligation, respectively. PGI-2 production rose immediately after partial portal ligation from 62 +- 10 to 164 +- 4.1 ng/min/100 gm and remained elevated thereafter. Conclusions. The mechanism for elevated PGI-2 in acute PHT is unclear, but in chronic and long-term PHT, it is probably due in part to increased splanchnic PGI? production.