Response of the Trilaminar Retinal Vessel Network to Intraocular Pressure Elevation in Rat Eyes.
Journal
Investigative ophthalmology & visual science
ISSN: 1552-5783
Titre abrégé: Invest Ophthalmol Vis Sci
Pays: United States
ID NLM: 7703701
Informations de publication
Date de publication:
07 02 2020
07 02 2020
Historique:
entrez:
8
2
2020
pubmed:
8
2
2020
medline:
14
4
2020
Statut:
ppublish
Résumé
The purpose of this study was to test the hypothesis that the superficial, intermediate, and deep retinal vascular plexus show different responses to intraocular pressure (IOP) elevation. Anesthetized adult Long Evans rats (n = 14) were imaged using optical coherence tomography angiography (OCTA; Spectralis) at baseline (IOP 10 mm Hg) and in follow-up mode to examine the vasculature during IOP elevation (10 to 110 mm Hg, 10 mm Hg steps, each step 3 minutes). A 20° × 10° field was imaged. Vessel density within a 2D projection image was determined (%) for the superficial vascular complex (SVC), intermediate capillary plexus (ICP), and deep capillary plexus (DCP). Comparisons were made between layers using 2-way repeated measures ANOVA (layer versus IOP) following normalization to baseline (% relative to 10 mm Hg). The three vascular layers responded differently to IOP elevation. For IOPs between 40 and 60 mm Hg, DCP and ICP capillaries were significantly more resistant to IOP elevation than those in the SVC. When IOP was elevated above 70 mm Hg, all layers showed reduced vessel density. IOP induced change in SVC vessel density closely followed reductions in thickness of the inner retinal layers (nerve fiber, ganglion cell, and inner plexiform layer). This close relationship between reductions in tissue thickness and vessel density was less apparent for the ICP and DCP. These data show that the intermediate and deep vascular plexus in the rat retina have a greater capacity for autoregulation against mild IOP elevation but are more affected at high IOP.
Identifiants
pubmed: 32031574
pii: 2760831
doi: 10.1167/iovs.61.2.2
pmc: PMC7325622
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2Subventions
Organisme : NEI NIH HHS
ID : R01 EY019939
Pays : United States
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