title: Vasodilatory effects of antivascular endothelium growth factor (VEGF) antibody, corticosteroid, and nitric oxide on the posterior ciliary arteries.
abstract: OBJECTIVE
  The purpose of this study was to determine whether an antivascular endothelium growth factor (VEGF) antibody, a corticosteroid, and sodium nitroprusside (SNP) [a nitric oxide (NO) donor] are possible treatment agents for nonarteritic ischemic optic neuropathy (NAION) by clarifying their effects on high-K (potassium) solution-induced contraction in isolated rabbit and human posterior ciliary arteries (PCA).
  
  
  METHODS
  Vascular ring segments were cut from the distal section of the PCA and mounted in a double-myograph system. After obtaining the maximal contraction following the administration of high-K solution, bevacizumab as an anti-VEGF antibody, methylprednisolone as a corticosteroid, and SNP were administered separately. When a vasodilatory effect was observed, carboxy-PTIO (a NO scavenger) or L-NAME (a NO synthase inhibitor) was administered.
  
  
  RESULTS
  Bevacizumab did not relax either the rabbit or the human PCA, whereas methylprednisolone relaxed both. Neither carboxy-PTIO nor L-NAME inhibited methylprednisolone-induced relaxation. SNP relaxed the rabbit PCA. Carboxy-PTIO inhibited SNP-induced relaxation, but L-NAME did not. In the human PCA, the vasodilatory effect of SNP was present, but weaker than in the rabbit PCA.
  
  
  CONCLUSIONS
  A corticosteroid has NO-independent vasodilatory effects. Exogenous NO has a weak dilating effect in the human PCA. Therefore, corticosteroid could be effective for the treatment of NAION.
authors.affiliation: Department of Ophthalmology, Faculty of Medicine, University of Miyazaki, 5200 Kihara Kiyotake, Miyazaki, Miyazaki 889-1692, Japan. hchuman@post.med.miyazaki-u.ac.jp
authors.forename: Hideki
authors.initials: H
authors.lastname: Chuman
authors.forename: Naoko
authors.initials: N
authors.lastname: Kawano
authors.forename: Maki
authors.initials: M
authors.lastname: Kozawa
authors.forename: Nobuhisa
authors.initials: N
authors.lastname: Nao-I
mesh_terms: D000305:Adrenal Cortex Hormones / Q000494:pharmacology*; D000818:Animals; D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology*; D000068258:Bevacizumab; D019842:Ciliary Arteries / Q000187:drug effects / Q000503:physiopathology*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D045462:Endothelium-Dependent Relaxing Factors / Q000494:pharmacology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000494:pharmacology*; D018917:Optic Neuropathy, Ischemic / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D011817:Rabbits; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis* / Q000037:antagonists & inhibitors; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000305:Adrenal Cortex Hormones; D061067:Antibodies, Monoclonal, Humanized; D045462:Endothelium-Dependent Relaxing Factors; D042461:Vascular Endothelial Growth Factor A; D014665:Vasodilator Agents; D000068258:Bevacizumab; D009569:Nitric Oxide