Ocular blood flow and systemic blood pressure in patients with primary open-angle glaucoma and ocular hypertension.

PURPOSE: There is evidence that altered optic nerve head (ONH) blood flow may play a role in the development and progression of glaucoma. In the present study, the baseline characteristics were examined in a study population participating in a clinical trial in which the ocular hemodynamic effects of timolol and dorzolamide were compared. METHODS: One hundred forty patients with primary open-angle glaucoma (POAG) or ocular hypertension (OHT) were included in this trial and their baseline parameters compared with those of a group of 102 age-matched control subjects. Scanning laser Doppler flowmetry was used to measure blood flow in the temporal neuroretinal rim and the cup of the ONH. Pulsatile choroidal blood flow was assessed by laser interferometric measurement of fundus pulsation amplitude. In addition, hemodynamic parameters and mean arterial pressure were calculated in both groups. RESULTS: All ocular hemodynamic parameters were significantly lower in the POAG/OHT group compared with the healthy control group (P < 0.001 each). In addition, a significant positive correlation between laser Doppler flowmetry readings and mean arterial pressure was observed in patients with glaucoma but not in healthy control subjects. Likewise, the correlation coefficient between fundus pulsation amplitude and mean arterial pressure was higher in patients with glaucoma than in healthy control subjects. CONCLUSIONS: The present study indicates reduced ONH and choroidal blood flow and an abnormal association between blood pressure and ocular perfusion in patients with primary open-angle glaucoma or ocular hypertension, independent of topical antiglaucoma medication. Hence, vascular dysregulation appears to be an early manifestation in glaucoma that is not caused by pharmacologic intervention.

Changes in choroidal blood flow during light/dark transitions are not altered by atropine or propranolol in healthy subjects.

It has recently been reported that light/dark transitions lead to changes in choroidal blood flow. Several observations indicate that these changes in choroidal perfusion are triggered at least in part by neural mechanisms. In the present study we hypothesised that the choroidal blood flow response to changes in retinal illumination may be modified by either the muscarinic receptor antagonist atropine or by the beta-receptor antagonist propranolol. In 15 healthy subjects the response of choroidal perfusion was studied in a randomised placebo-controlled three way cross-over study using laser Doppler flowmetry and laser interferometric measurement of fundus pulsation amplitude. Before drug administration a transition from light to dark reduced both choroidal haemodynamic parameters by 8%-12%. Neither propranolol nor atropine altered basal choroidal blood flow or choroidal blood flow responses to light/dark transitions. Our data indicate that neither muscarinic nor beta-receptors are involved in the choroidal blood flow response to changes in retinal illumination. Further studies are required to elucidate which mechanisms contribute to this blood flow behaviour of the choroid.