title: Expression of cyclooxygenase in hyperdynamic portal hypertensive rats.
abstract: BACKGROUND
  By detecting hemodynamic changes, concentration of plasm prostacyclin (PGI2) and expression of cyclooxygenase (COX) in vasculature and splanchnic tissues, we evaluated the relative contributions of PGI2 and COX mRNA expression to the hyperdynamic circulatory state in chronic portal hypertensive rats.
  
  
  METHODS
  Fifty male Sprague-Dawley rats were divided into 3 groups: intrahepatic portal hypertension (IHPH, n=18) by injection of CCl4, prehepatic portal hypertension (PHPH, n=18) by partial stenosis of the portal vein, and sham-operated controls (SO, n=14). Splanchnic hemodynamics was measured by radioactive microsphere techniques and the concentration of PGI2 was detected by specific radioimmunoassay for its stable hydrolysis product 6-keto-PGF1alpha. Semi-quantitive reverse transcriptase-polymerase chain reaction (RT-PCR) was performed to measure the levels of COX-1 mRNA and COX-2 mRNA in the thoracic aorta, superior mesenteric artery (SMA), and small intestine of IHPH, PHPH and SO rats, respectively.
  
  
  RESULTS
  Hyperdynamic circulatory state was characterized by increased splanchnic blood flow and decreased splanchnic vascular resistance in IHPH and PHPH rats. The concentration of plasma 6-keto-PGF1alpha (pg/ml) in IHPH (1093.75+/-142.15) and PHPH (897.42+/-53.29) rats was significantly higher than that in SO rats (730.13+/-98.67) (P<0.05). The expression of COX-1 mRNA in the thoracic aorta, SMA and small intestine was enhanced, whereas COX-2 mRNA expression was not detected in either of these vessels or the small intestine. The plasma 6-keto-PGF1alpha concentration and the expression of COX-1 mRNA in these vessels and the small intestine were closely correlated with such hemodynamic parameters as portal venous inflow (PVI), splanchnic vascular resistance (SVR) and free portal venous pressure (FPP) (P<0.05).
  
  
  CONCLUSIONS
  The expression of COX-1 mRNA and the levels of PGI2 were closely related to the hyperdynamic circulatory state of portal hypertensive rats.
authors.affiliation: Department of Surgery, Renji Hospital, Shanghai Second Medical University, Shanghai 200127, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Cao
authors.forename: Jia
authors.initials: J
authors.lastname: Xu
authors.forename: Rong
authors.initials: R
authors.lastname: Hua
authors.forename: Fang-Bin
authors.initials: FB
authors.lastname: Meng
authors.forename: Jiang-Feng
authors.initials: JF
authors.lastname: Qiu
authors.forename: Zhi-Yong
authors.initials: ZY
authors.lastname: Wu
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001483:Base Sequence; D004195:Disease Models, Animal; D011464:Epoprostenol / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation; D005819:Genetic Markers; D006975:Hypertension, Portal / Q000175:diagnosis* / Q000235:genetics; D008297:Male; D008969:Molecular Sequence Data; D011336:Probability; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity
chemical_list: D005819:Genetic Markers; D012333:RNA, Messenger; D011464:Epoprostenol; D011451:Prostaglandin-Endoperoxide Synthases