Vasodilatory effects of antivascular endothelium growth factor (VEGF) antibody, corticosteroid, and nitric oxide on the posterior ciliary arteries
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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).
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.
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.
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.
KeywordsAnti-VEGF antibody Corticosteroid Nitric oxide Posterior ciliary artery Vasodilatory effect
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