Purchase this article with an account.
Susannah Waxman, Chao Wang, Yalong Dang, Ying Hong, Hamed Esfandiari, Priyal Shah, Kira L. Lathrop, Ralitsa T. Loewen, Nils A. Loewen; Structure–Function Changes of the Porcine Distal Outflow Tract in Response to Nitric Oxide. Invest. Ophthalmol. Vis. Sci. 2018;59(12):4886-4895. doi: 10.1167/iovs.18-24943.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To correlate outflow function and outflow tract vessel diameter changes induced by nitric oxide (NO).
In a porcine anterior segment perfusion model, the effects of a nitric oxide donor (100 μM DETA-NO) on outflow facility were compared with controls (n = 8 per group) with trabecular meshwork (TM) and after circumferential ab interno trabeculectomy (AIT). Outflow structures were assessed with spectral-domain optical coherence tomography (SD-OCT) before and after NO, or an NO synthase inhibitor (100 μM L-NAME) and the vasoconstrictor, endothelin-1 (100 pg/mL ET-1). Scans were processed with a custom macroscript and aligned for automated reslicing and quantification of cross-sectional outflow tract areas (CSA).
The facility increased after DETA-NO (Δ of 0.189 ± 0.081 μL/min·mm Hg, P = 0.034) and AIT (Δ of 0.251 ± 0.094 μL/min·mm Hg, P = 0.009), respectively. Even after AIT, DETA-NO increased the facility by 61.5% (Δ of 0.190 ± 0.074 μL/min·mm Hg, P = 0.023) and CSA by 13.9% (P < 0.001). L-NAME + ET-1 decreased CSA by −8.6% (P < 0.001). NO increased the diameter of focal constrictions 5.0 ± 3.8-fold.
NO can dilate vessels of the distal outflow tract and increase outflow facility in a TM-independent fashion. There are short, focally constricting vessel sections that display large diameter changes and may have a substantial impact on outflow.
This PDF is available to Subscribers Only