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      Laser Cyclophotocoagulation Enhances the Regulative Capacity of Retinal Vessels in Glaucoma

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          Abstract

          Purpose:

          To determine the effects of laser surgical IOP reduction by means of transscleral cyclophotocoagulation (CPC) on retinal blood flow parameters in glaucoma patients using Dynamic Vessel Analysis (DVA).

          Materials and Methodology:

          26 patients (average age: 70 years) with a long history of primary open angle glaucoma underwent CPC. The effect on the reactive capacity of retinal vessels was assessed before and 6-8 weeks after CPC by means of the Dynamic Vessel Analyzer (DVA) using flicker light provocation.

          Results:

          In our group of POAG patients, IOP was significantly reduced about approximately 20% by CPC while systemic blood pressure and heart rate were not changed.

          The most obvious differences between the pre- and postoperative DVA measurements could be observed in the maximal dilation of the retinal arteries which increased from 0.75 % (+/- 0.6) to 3.17 % (+/- 0.5) with an average increase of 2.4 % (p<0.01). In addition, the ability of the arteries for constriction improved significantly (p<0.05) while the dynamic responses of the veins and the initial baseline values (MU) of the vessel diameters did not change.

          Conclusions:

          Our results of DVA measurements after an IOP-lowering laser surgical intervention (CPC) reveal a significant recovery of the regulative capacity of retinal arteries in glaucoma patients that has up to now neither been properly documented nor appreciated. Future studies with long-term follow-up must determine the clinical importance of these findings for the treatment of glaucoma patients.

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          Most cited references25

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          Use of the retinal vessel analyzer in ocular blood flow research.

          The present article describes a standard instrument for the continuous online determination of retinal vessel diameters, the commercially available retinal vessel analyzer. This report is intended to provide informed guidelines for measuring ocular blood flow with this system. The report describes the principles underlying the method and the instruments currently available, and discusses clinical protocol and the specific parameters measured by the system. Unresolved questions and the possible limitations of the technique are also discussed. © 2009 The Authors. Journal compilation © 2009 Acta Ophthalmol.
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            Autoregulation, a balancing act between supply and demand.

            Regulation of blood flow is necessary to adapt to different conditions. Regulation of ocular blood flow (OBF) compensates for varying perfusion pressures (autoregulation), adapts to the retinal activity (neurovascular coupling), and keeps the back of the eye at constant temperature (thermoregulation). While all vessels are under the control of the vascular endothelial cells, the retinal vessels are additionally under the control of the neural and glial cells, and the choroidal vessels are influenced by the autonomic nervous system. The optic nerve head is additionally controlled by circulating hormones. If the regulation does not occur according to the needs of the tissue, it is referred to as vascular dysregulation. Such a dysregulation can be secondary in nature, as, for example, in multiple sclerosis, in which the high level of endothelin reduces OBF. Dysregulation, however, can also occur without any underlying disease and is characterized by an inborn tendency to respond differently to various stimuli, such as cold temperatures or mechanical or emotional stress. The constellation of these features is known as primary vascular dysregulation (PVD). Subjects with PVD have disturbed autoregulation leading to an unstable OBF. This instability, in turn, induces a repeated mild reperfusion injury. The resulting oxidative stress contributes to the pathogenesis of glaucomatous optic neuropathy.
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              Response of retinal vessel diameters to flicker stimulation in patients with early open angle glaucoma.

              Diffuse luminance flicker increases retinal vessel diameters in animals and humans, indicating the ability of the retina to adapt to different metabolic demands. The current study seeks to clarify whether flicker-induced vasodilatation of retinal vessels is diminished in glaucoma patients. Thirty-one patients with early stage glaucoma (washout for antiglaucoma medication) and 31 age- and sex- matched healthy volunteers were included in the study. Retinal vessel diameters were measured continuously with a Retinal Vessel Analyzer. During these measurements three episodes of square wave flicker stimulation periods (16, 32, and 64 secs; 8 Hz) were applied through the illumination pathway of the retinal vessel analyser. Flicker-induced vasodilatation in retinal veins was significantly diminished in glaucoma patients as compared with healthy volunteers (ANOVA, P < 0.01). In healthy volunteers, retinal venous vessel diameters increased by 1.1 +/- 1.8% (16 seconds, P < 0.001), 2.0 +/- 2.6 (32 seconds, P < 0.001), and 2.1 +/- 2.1% (64 seconds, P < 0.001) during flicker stimulation. In glaucoma patients, venous vessel diameters increased by 0.2 +/- 1.7% (16 seconds, P < 0.6), 1.1 +/- 2.1% (32 seconds, P < 0.01), and 0.8 +/- 2.5 (64 seconds, P < 0.09). In retinal arteries, no significant difference in flicker response was noticed between the two groups (ANOVA, P < 0.6). In healthy controls, flicker stimulation increased retinal arterial vessel diameters by 1.0 +/- 2.4% (P < 0.03), 1.6 +/-3.2% (P < 0.004) and 2.4 +/- 2.6% (P < 0.001) during 16, 32, and 64 seconds of flicker, respectively. In glaucoma patients, flickering light changed arterial vessel diameters by 0.3 +/-2.6% (16 seconds, P = 0.4), 1.3 +/-3.1% (32 seconds, P = 0.03), and 1.8 +/- 3.8% (64 seconds, P = 0.005). Flicker-induced vasodilatation of retinal veins is significantly diminished in patients with glaucoma compared with healthy volunteers. This indicates that regulation of retinal vascular tone is impaired in patients with early glaucoma, independently of antiglaucoma medication.
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                Author and article information

                Journal
                Open Ophthalmol J
                Open Ophthalmol J
                TOOPHTJ
                The Open Ophthalmology Journal
                Bentham Open
                1874-3641
                13 June 2014
                2014
                : 8
                : 27-31
                Affiliations
                [1 ]Department of Ophthalmology, Evangelische Kliniken Gelsenkirchen, Munckelstr. 27, 45879 Gelsenkirchen, Germany
                [2 ]Department of Ophthalmology, University of Duisburg-Essen, Hufelandstr. 55, 45122 Essen, Germany
                [3 ]Institut of Biomedical Engineering and Informatics, Ilmenau University of Technology, Ilmenau, Gustav-Kirchhoff-Str.2, Germany
                [4 ]Imedos Systems UG, Jena, Am Naßtal 4, Germany
                Author notes
                [* ]Address correspondence to this author at the Department of Ophthalmology, Evangelische Kliniken Gelsenkirchen, Munckelstr. 27, 45879 Gelsen-kirchen, Germany; Tel: 0049 – 209 – 37261; Fax: 0049 – 209 – 378555; E-mail: stephan.kremmer@ 123456arcor.de
                Article
                TOOPHTJ-8-27
                10.2174/1874364101408010027
                4110390
                25067978
                6e247ab8-3be3-455a-9ad7-92ba1688df9b
                © Kremmer et al.; Licensee Bentham Open.

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 11 December 2013
                : 6 May 2014
                : 22 May 2014
                Categories
                Article

                Ophthalmology & Optometry
                cyclophotocoagulation (cpc),glaucoma,iop,retinal vessel autoregulation,dynamic vessel analyzer (dva),vascular dysregulation.

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