title: Effects of tetramethylpyrazine on prostaglandin E(2)- and prostaglandin E(2) receptor agonist-induced disruption of blood-aqueous barrier in pigmented rabbits.
abstract: OBJECTIVE
  To evaluate the effect of tetramethylpyrazine on the elevation of aqueous flare and intraocular pressure (IOP) induced by prostaglandin (PG) E(2) and PGE(2) receptor (EP) agonists.
  
  
  METHODS
  PGE(2) or EP agonists (11-deoxy PGE(1), EP(2) agonist; 17-phenyl trinor PGE(2), EP(1) and EP(3) agonist; or sulprostone, EP(1) and EP(3) agonist), 25 microg/mL, were transcorneally administered to pigmented rabbits. Animals were pretreated with tetramethylpyrazine intravenously (10 or 30 mg/kg) or topically (0.1% solution). Aqueous flare was measured using a laser flare-cell meter, and the intensity was expressed as the area under the curve (AUC). Intraocular pressure was measured using a noncontact tonometer.
  
  
  RESULTS
  After administration of PGE(2), aqueous flare and IOP increased and then gradually decreased. The AUC of eyes pretreated with tetramethylpyrazine, 10 or 30 mg/kg, intravenously, or topical 0.1% solution, was significantly smaller than that of the controls. The mean Delta IOP of eyes pretreated with tetramethylpyrazine, 30 mg/kg intravenously, was significantly lower than that of the controls. After administration of 11-deoxy PGE(1), aqueous flare increased and then gradually decreased. 17-phenyl trinor PGE(2) and sulprostone did not disrupt the blood-aqueous barrier. The AUC of eyes pretreated with tetramethylpyrazine, 10 or 30 mg/kg, intravenously, before 11-deoxy PGE(1) application was significantly smaller than that of the controls.
  
  
  CONCLUSIONS
  The results indicated that tetramethylpyrazine inhibited PGE(2)- or 11-deoxy PGE(1)-induced elevation of aqueous flare and IOP.
authors.affiliation: Department of Ophthalmology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kitagawa
authors.forename: S
authors.initials: S
authors.lastname: Hayasaka
authors.forename: Y
authors.initials: Y
authors.lastname: Nagaki
authors.forename: K
authors.initials: K
authors.lastname: Watanabe
mesh_terms: D000527:Alprostadil / Q000031:analogs & derivatives* / Q000633:toxicity; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001082:Aqueous Humor / Q000187:drug effects* / Q000378:metabolism; D018916:Blood-Aqueous Barrier / Q000187:drug effects*; D015232:Dinoprostone / Q000031:analogs & derivatives* / Q000633:toxicity*; D007429:Intraocular Pressure / Q000187:drug effects*; D008297:Male; D011719:Pyrazines / Q000494:pharmacology*; D011817:Rabbits; D018078:Receptors, Prostaglandin E / Q000819:agonists*; D014606:Uveitis, Anterior / Q000378:metabolism / Q000517:prevention & control*
chemical_list: C092396:17-phenyltrinorprostaglandin E2; D000894:Anti-Inflammatory Agents, Non-Steroidal; D011719:Pyrazines; D018078:Receptors, Prostaglandin E; C016767:sulprostone; D000527:Alprostadil; D015232:Dinoprostone; C034008:11-deoxyprostaglandin E1; C017953:tetramethylpyrazine