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Editors Selection IGR 7-3

Blood Flow: Role of L-arginine/NO system

Comment by Alon Harris on:

22695 Role of NO in the control of choroidal blood flow during a decrease in ocular perfusion pressure, Simader C; Lung S; Weigert G et al., Investigative Ophthalmology and Visual Science, 2009; 50: 372-377

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Various hemodynamic deficits continue to be identified in patients with glaucomatous optic neuropathy. The underlying vascular mechanisms controlling perfusion pressure and ocular blood flow are important considerations in glaucoma. The current study by Simader et al. (210) investigates the role of the L-arginine/nitric oxide system in the role of choroidal blood flow regulation during a decrease in ocular perfusion pressure. The authors present interesting data which confirm previously published observations that the choroid shows some regulatory capacity during reduced perfusion pressure and suggest the L-arginine/nitric oxide-system plays a role in the maintenance of basal vascular tone but is not involved in the choroidal response when intraocular pressure is increased. A strength of the current study is the use of α-receptor agonist (phenylephrine) as a control substance to induce comparable effects on blood pressure seen during systemic administration of L-NMMA.

Numerous population based studies continue to link ocular perfusion pressure to the presence, incidence and progression of glaucoma

The strict inclusion criteria including history and physical examination, 12- lead electrocardiogram; CBC; clinical blood chemistry and serology and ophthalmic examination also benefit the study data. The application of the current study results to glaucoma patients however is mitigated by the study participants age and healthy status (14 healthy males aged 25 ± 4 years). Vascular autoregulation of an elderly glaucomatous population likely differs greatly from healthy young males. Another limitation is the use of only laser Doppler flowmetry for measurements of subfoveal choroid hemodynamics (in arbitrary units). As retinal and other vascular tissues were not assessed, a blood flow steal phenomenon cannot be ruled out. In this capacity blood flow may have been redirected from the choroid to vital retinal and optic nerve tissues during decreases in ocular perfusion pressure. Finally, IOP and choroidal parameters could not be assessed simultaneously. Acknowledging these limitations, the results of this study contribute to our understanding of vascular autoregulation during dynamic shifts in ocular perfusion pressure. As numerous population based studies continue to link ocular perfusion pressure to the presence, incidence and progression of glaucoma, it is essential to reveal the vascular mechanisms of ocular blood flow regulation.

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