title: Prostacyclin production in acute, chronic, and long-term experimental portal hypertension.
abstract: BACKGROUND
  Chronic portal hypertension (PHT) is characterized by a high portosystemic shunt (PSS) and increased splanchnic blood flow. It has been suggested that the splanchnic vasodilator, prostacyclin (PGI2), mediates this increased flow. We studied splanchnic PGI2 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 PGI2 in PHT.
  
  
  METHODS
  Levels of 6-keto prostaglandin F1 alpha 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 PGI2 production (PGI2 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 < 0.001). Splanchnic blood flow initially fell from 84 +/- 4.8 to 37.4 +/- 7 ml/min/100 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. PGI2 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 PGI2 in acute PHT is unclear, but in chronic and long-term PHT, it is probably due in part to increased splanchnic PGI2 production.
authors.affiliation: Department of Surgery, Johns Hopkins Hospital, Baltimore, MD 21205.
authors.forename: J V
authors.initials: JV
authors.lastname: Sitzmann
authors.forename: K
authors.initials: K
authors.lastname: Campbell
authors.forename: Y
authors.initials: Y
authors.lastname: Wu
authors.forename: C
authors.initials: C
authors.lastname: St Clair
mesh_terms: D000208:Acute Disease; D000818:Animals; D002908:Chronic Disease; D003097:Collateral Circulation; D011464:Epoprostenol / Q000097:blood* / Q000502:physiology; D006940:Hyperemia / Q000209:etiology* / Q000378:metabolism; D006975:Hypertension, Portal / Q000150:complications / Q000503:physiopathology*; D008026:Ligation; D016014:Linear Models; D017082:Portal Pressure; D011817:Rabbits; D013152:Splanchnic Circulation / Q000502:physiology*; D013154:Spleen / Q000098:blood supply / Q000503:physiopathology; D014655:Vascular Resistance
chemical_list: D011464:Epoprostenol