title: [The effect of PGI2 on formation and development of hyperdynamic circulatory state in portal hypertensive rats].
abstract: OBJECTIVE
  To investigate the effects of prostacyclin (PGI(2)) and nitric oxide (NO) in the development of hyperdynamic circulatory state on chronic portal hypertensive rats.
  
  
  METHODS
  Sixty-six male SD rats were divided into three groups, namely intrahepatic portal hypertension (IHPH) by injection of CCl(4), prehepatic portal hypertension (PHPH) by partial stenosis of the portal vein for 2 weeks and sham-operated controls (SO). Animals in each group were divided further into 3 subgroups and received N(omega)-nitro-L-arginine (L-NNA), indomethacin and saline (as control), respectively. Splanchnic and systemic hemodynamics was measured using radioactive microsphere techniques. The NO concentration in serum was determined by nitrates-nitrites which were measured using a colorimetric method, and concentration of PGI(2) was determined using specific radioimmunoassay for its stable hydrolytic product, 6-keto-PGF(1 alpha).
  
  
  RESULTS
  The concentrations of plasma 6-keto-PGF(1 alpha) and serum nitrates + nitrites in IHPH rats (1 123.85 +/- 153.64; 73.34 +/- 4.31) and in PHPH rats (891.88 +/- 83.11; 75.21 +/- 6.89) were significantly higher than those of SO rats (725.53 +/- 105.54;58.79 +/- 8.47). L-NNA and indomethacin could decrease the concentrations of plasma 6-keto-PGF(1 alpha) and serum nitrates + nitrites in IHPH and PHPH rats (P < 0.05). At the same time, CI, FPP and PVI were lowered while MAP, TPR and SVR were increased (P < 0.05). After deduction of NO action, there were no significant correlation between plasma PGI(2) level and hemodynamic parameters such as CI, TPR, PVI and SVR. However, after deduction of PGI(2) action, NO was still correlated highly with those hemodynamic parameters.
  
  
  CONCLUSIONS
  It is NO rather then PGI(2) that is a mediator in the formation and development of hyperdynamic circulatory state in chronic portal hypertensive rats.
authors.affiliation: Department of General Surgery, Renji Hospital, Shanghai Second Medical University, Shanghai 200127, China.
authors.forename: Zhi-yong
authors.initials: ZY
authors.lastname: Wu
authors.forename: Xue-song
authors.initials: XS
authors.lastname: Chen
authors.forename: Hui
authors.initials: H
authors.lastname: Cao
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology; D011464:Epoprostenol / Q000097:blood / Q000502:physiology*; D006439:Hemodynamics / Q000187:drug effects; D006975:Hypertension, Portal / Q000097:blood / Q000503:physiopathology*; D008297:Male; D009569:Nitric Oxide / Q000097:blood / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000097:blood; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D019335:Nitroarginine; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D019001:Nitric Oxide Synthase