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Review
. 2013 Feb;13(1):36-42.
doi: 10.1016/j.coph.2012.09.003. Epub 2012 Sep 23.

Ocular perfusion pressure and ocular blood flow in glaucoma

Affiliations
Review

Ocular perfusion pressure and ocular blood flow in glaucoma

A Popa Cherecheanu et al. Curr Opin Pharmacol. 2013 Feb.

Abstract

Glaucoma is a progressive optic neuropathy of unknown origin. It has been hypothesized that a vascular component is involved in glaucoma pathophysiology. This hypothesis has gained support from studies showing that reduced ocular perfusion pressure is a risk factor for the disease. The exact nature of the involvement is, however, still a matter of debate. Based on recent evidence we propose a model including primary and secondary insults in glaucoma. The primary insult appears to happen at the optic nerve head. Increased intraocular pressure and ischemia at the post-laminar optic nerve head affects retinal ganglion cell axons. Modulating factors are the biomechanical properties of the tissues and cerebrospinal fluid pressure. After this primary insult retinal ganglion cells function at a reduced energy level and are sensitive to secondary insults. These secondary insults may happen if ocular perfusion pressure falls below the lower limit of autoregulation or if neurovascular coupling fails. Evidence for both faulty autoregulation and reduced hyperemic response to neuronal stimulation has been provided in glaucoma patients. The mechanisms appear to involve vascular endothelial dysfunction and impaired astrocyte-vessel signaling. A more detailed understanding of these pathways is required to direct neuroprotective strategies via the neurovascular pathway.

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Figures

None
Graphical abstract
Figure 1
Figure 1
A model of primary and secondary insults in glaucoma and the involvement of low ocular perfusion pressure (OPP). The primary insult occurs at the optic nerve head owing to increased intraocular pressure (IOP) and optic nerve head (ONH) ischemia. Reduced cerebrospinal fluid (CSF) pressure and the biomechanical properties of ocular tissues modify susceptibility. In primary open angle glaucoma (POAG) retinal ganglion cells (RGCs) then function at reduced energy states with affected mitochondria. Oxidative stress due to reactive oxygen species (ROS) and secondary insults such as abnormal autoregulation of abnormal neurovascular coupling can lead to RGC death.
Figure 2
Figure 2
Abnormal autoregulation in glaucoma and factors that may contribute. Primary vascular dysregulation, endothelial dysfunction, astrocyte activation and increased intraocular pressure induce compromised autoregulation leading to abnormal pressure-flow relationship. Periods of ischemia are then more likely to occur when ocular perfusion pressure (OPP) is reduced, when OPP fluctuates and when intraocular pressure (IOP) is increased.
Figure 3
Figure 3
Abnormal neurovascular coupling in glaucoma and factors that may contribute. Primary vascular dysregulation, endothelial dysfunction, astrocyte activation and neuronal dysfunction induce compromised neurovascular coupling. This will lead to periods of reduced nutrient supply (including oxygen and glucose) during neuronal stimulation. Such periods are more likely to occur when ocular perfusion pressure (OPP) is reduced or when OPP fluctuates.
Figure 4
Figure 4
Neuroprotective strategies need not only to consider the neurodegenerative loss of RGCs, but also neurovascular and neuroinflammatory components.

References

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