title: Effects of somatostatin and octreotide on portal-systemic collaterals in portal hypertensive rats.
abstract: OBJECTIVE
  Somatostatin and its long-acting analogue, octreotide, have been used to cease variceal bleeding with uncertain mechanisms. This study investigated whether somatostatin and octreotide have a direct vasoconstrictive effect on the portal-systemic collaterals of portal-hypertensive rats and potentiate the vasoconstriction induced by endothelin-1 in these vascular beds.
  
  
  METHODS
  The vascular responses of collateral vessels to graded concentrations of somatostatin (10(-9)-10(-5) mol/l), octreotide (10(-10)-10(-6) mol/l), norepinephrine (10(-9)-10(-5) mol/l) and vehicle (Krebs solution) were evaluated in perfused collateral vascular beds of rats with portal hypertension induced by partial portal vein ligation. In addition, the perfusion pressure changes of collateral vessels to endothelin-1 (10(-8) mol/l) in the presence of vehicle(control), somatostatin (10(-6) mol/l) and octreotide (10(-6) mol/l) were tested.
  
  
  RESULTS
  Compared with the vehicle group, norepinephrine significantly increased the perfusion pressure of collateral vessels at concentrations between 10(-7) and 10(-5) mol/l. In contrast, neither somatostatin nor octreotide significantly changed the perfusion pressure. Somatostatin and octreotide significantly enhanced the endothelin-1-induced vasoconstrictive effect on the collaterals.
  
  
  CONCLUSIONS
  Somatostatin and octreotide exert no direct vasoconstrictive effect on the collateral vessels of portal hypertensive rats. In the presence of endothelin-1, somatostatin and octreotide exert a local vasoconstrictive effect on these vascular beds.
authors.affiliation: Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital, No-201, Sec 2, Shih-Pai Road, Taipei 11217, Taiwan, ROC.
authors.forename: Hui-Chun
authors.initials: HC
authors.lastname: Huang
authors.forename: Fa-Yauh
authors.initials: FY
authors.lastname: Lee
authors.forename: Che-Chang
authors.initials: CC
authors.lastname: Chan
authors.forename: Full-Young
authors.initials: FY
authors.lastname: Chang
authors.forename: Sun-Sang
authors.initials: SS
authors.lastname: Wang
authors.forename: Han-Chieh
authors.initials: HC
authors.lastname: Lin
authors.forename: Ming-Chih
authors.initials: MC
authors.lastname: Hou
authors.forename: Chien-Ting
authors.initials: CT
authors.lastname: Chen
authors.forename: Chun-Ching
authors.initials: CC
authors.lastname: Tai
authors.forename: I-Nien
authors.initials: IN
authors.lastname: Lai
authors.forename: Shou-Dong
authors.initials: SD
authors.lastname: Lee
mesh_terms: D000818:Animals; D003097:Collateral Circulation / Q000187:drug effects*; D019332:Endothelin-1 / Q000494:pharmacology; D006490:Hemostatics / Q000494:pharmacology*; D006975:Hypertension, Portal / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D015282:Octreotide / Q000494:pharmacology*; D011168:Portal System / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013004:Somatostatin / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D019332:Endothelin-1; D006490:Hemostatics; D013004:Somatostatin; D015282:Octreotide