Vasodilatory effects of antivascular endothelium growth factor (VEGF) antibody, corticosteroid, and nitric oxide on the posterior ciliary arteries.

Purpose: 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.