The local determinants of blood fl ow through the ocular circulations include both passive and active mechanisms. The most obvious passive mechanism is the compressing force exerted by the intraocular pressure (IOP) on the intraocular blood vessels, particularly the veins. By contrast, the active “local control” mechanisms in the ocular circulations are more diffi cult to defi ne. Based on other tissues with more accessible circulations, the possible local control mechanisms include vascular responses linked to nearby tissue metabolism (e.g., reactive hyperemia, functional hyperemia, and autoregulation), transmural pressure (e.g., myogenic response, reactive hyperemia, and autoregulation), shear stress (fl ow-dependent vasodilation), and intercellular conduc tion. The relative contributions of these active mechanisms in the ocular circulations are hard to defi ne given the complex vascular organization and relative inaccessibility. Ocular blood fl ow measurement is technically challenging, and discrete perturbations that elicit unambiguous responses characteristic of a particular mechanism in a single vascular bed are diffi cult to achieve. Eliminating confounding neurohumoral inputs is a further, though not insurmountable, challenge. For these reasons, we can often infer that a blood fl ow response in an ocular circulation is locally mediated, but the relative contributions of the underlying local control mechanisms are ill-defi ned. Nonetheless, there is evidence of local control behavior in the prelaminar optic nerve, choroid, retina, ciliary body, and iris.
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