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Editors Selection IGR 9-2
Basic Science: Autoregulation of ONH blood flow
Comment by Alon Harris on:
57185 Longitudinal alterations in the dynamic autoregulation of optic nerve head blood flow revealed in experimental glaucoma, Wang L; Cull G; Burgoyne CF et al., Investigative Ophthalmology and Visual Science, 2014; 55: 3509-3516
A complete understanding of the complex physiology of vascular regulation in ocular tissues remains enigmatic in glaucomatous optic neuropathy due to imaging specific modalities, location of measure, and various other methodological considerations. In an effort to advance our understanding of the dynamic nature of blood flow autoregulation during fluctuating perfusion pressure Wang and colleagues present a novel dynamic autoregulation (dAR) analysis to explore the hypothesis that the optic nerve head (ONH) blood flow autoregulation is disrupted during early stages of experimental glaucoma (EG) in non-human primates. The authors' work builds upon their previous finding that ONH blood flow is mildly increased during an early stage of EG and thereafter declines progressively in close correlation with the loss of retinal nerve fiber layer thickness. In the current investigation, the authors' dAR modeling focuses on the time course of the ONH blood flow response within the first 60 seconds after the IOP challenge, whereas their previous methodology (static autoregulation) was limited to a measurement window of after a three-minute or greater period of stabilization.
The authors' works depict a complex pattern of hemodynamic changes within the ONH after chronic IOP elevation
The authors found IOP predominates within the first few seconds, causing a steep blood flow decrease at a constant rate of decline; and after the initiation of autoregulation, equivalence was gradually reached at a given time point. The authors' works depict a complex pattern of hemodynamic changes within the ONH after chronic IOP elevation suggesting a biphasic, stage-dependent response and impaired dynamic autoregulation in EG. The authors should be congratulated, as their work is thoughtfully planned and very specific to a time course of autoregulation assessment not previously investigated. The authors' novel findings shed light on the complex and truly dynamic physiology of vascular response to fluctuating perfusion pressure and contributing ischemic insult to the ONH in glaucoma. One limitation of this investigation is that perfusion pressure may affect ONH blood flow differently if manipulations are induced by IOP variation compared to blood pressure fluctuations. Another factor to consider is the use of a single blood flow imaging technique (laser speckle imaging), which limits applicability of these results to the ONH without corresponding measures in the retina. Overall, these data provide an outstanding contribution to the field and the novel findings advance our understanding of vascular contributions to glaucomatous pathophysiology.
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