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Updated: Apr 18, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
Published on: March 12, 2016
Vascular dysregulation in normal-tension glaucoma is not affected by structure and function of the microcirculation
Jelle Bossuyt1, Gwendolijn Vandekerckhove, Tine L M De Backer
1From the Heymans Institute of Pharmacology (JB, TLMDB, SVV, MA, LMVB), Clinical Pharmacology, Ghent University; Department of Ophthalmology (GV, A-MS, PK, TR), Ghent University Hospital; Institute of Biomedical Technology (IBiTech) (PS), Ghent University, Ghent, Belgium; and Department of Internal Medicine (FV), Maastricht University Medical Centre, Maastricht, The Netherlands.
Abstract:
In normal-tension glaucoma (NTG), optic nerve damage occurs despite a normal intraocular pressure. Studies implicating systemic blood pressure or, more recently, arterial stiffness in the pathophysiology of NTG have produced conflicting results. Our aim was to investigate whether NTG is associated with alterations in the macrocirculation or microcirculation, cardiac function, and peripheral and central hemodynamics. Thirty patients with NTG (mean age 65 years, range 46-79) and 33 healthy subjects (mean age 67 years, range 42-79) matched for age and sex were included in the study. Exclusion criteria (for both cases and controls) were history of cardiovascular disease, diabetes mellitus, severe hypertension, and hypercholesterolemia. Aortic stiffness was measured using carotid-femoral pulse wave velocity (PWV), central hemodynamics using carotid artery applanation tonometry, and diameter, stiffness, and intima-media thickness (IMT) of the carotid and femoral artery using echo-tracking. Total peripheral resistance index (TPRI) was derived from mean arterial pressure and cardiac index, measured using ultrasound. There were no statistically significant differences in arterial structure nor function between NTG patients and age and sex-matched controls. NTG versus controls, respectively: brachial blood pressure 126 ± 15/77 ± 8 versus 127 ± 16/76 ± 7 mm Hg, P = 0.81; carotid-femoral PWV 9.8 ± 2.1 versus 10.1 ± 1.9 m/s, P = 0.60; TPRI 1833 ± 609 versus 1779 ± 602 dyne.s/cm5/m2, P = 0.79; and carotid IMT 0.65 ± 0.14 versus 0.68 ± 0.13 mm, P = 0.39. This study could not show an association of NTG with altered IMT, arterial stiffness, total peripheral resistance, cardiac output, and peripheral or central hemodynamics at rest. Although the majority of these NTG patients do exhibit symptoms of vascular dysregulation, in the present study this was not translated into alterations in the microcirculation or macrocirculation at rest.
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