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Received Oct 5, 2017; Accepted Nov 20, 2017
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1. Introduction
Autoregulatory mechanisms play very important roles in the control of blood flow in organ tissues to maintain oxygen and nutrition supply through vascular constriction or dilatation [1, 2]. Many studies have reported that autoregulation of optic nerve head (ONH) and choroidal blood flow occurs in response to a change in ocular perfusion pressure (OPP) [3–10].
In general, a role of vascular dysregulation and interaction of OPP and blood flow might be important factors in the eyes with glaucoma [2, 11]. It has been reported that there are circadian intraocular pressure (IOP) variations in healthy or glaucomatous eyes [12]. OPP is the difference between mean blood pressure (MBP) and IOP [2] and several investigators have demonstrated that the progression of glaucoma might be related to fluctuations in OPP [13, 14]. Sung et al. [15] reported that OPP fluctuations during 24 h might be significant predictors for the progression of the central visual field in eyes with normal tension glaucoma. Furthermore, Schmidl et al. [6] reported that impaired autoregulatory capacity was associated with both higher intraocular pressure (IOP) and higher mean blood pressure. However, the mechanism of autoregulation in the ONH blood flow has not been clarified in detail. Considering the above clinical findings, it is important to evaluate this mechanism.
Cull et al. [16] provided evidence for the association between ONH blood flow autoregulation and retinal nerve fiber layer thickness (RNFLT) loss. Another report demonstrated that the number of capillaries was lower in the temporal ONH quadrant than in the other ONH quadrants in monkey eyes with experimental glaucoma [17]. However, no study has elucidated whether there is a significant difference of autoregulatory capacity...
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