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L.R. Pasquale, G.T. Feke, M.N. Menke, M. Kuperwaser, J.W. McMeel; Effect of Brimonidine versus Latanoprost on the Maintenance of Retinal Blood Flow Homeostasis during Postural Change in Normal Tension Glaucoma . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1178.
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Purpose: We previously reported that the retinal hemodynamic response in healthy subjects to changes in posture (seated versus recumbent), with the attendant changes in retinal perfusion pressure, is characterized by arterial dilations or constrictions and concomitant blood speed changes that preserve retinal blood flow homeostasis. We have now applied the same experimental protocol to a group of patients with normal tension glaucoma (NTG) to determine whether retinal vascular dysregulation may occur. Methods: We used a Canon retinal laser Doppler blood flow instrument to measure the vessel diameter, blood speed, and blood flow rate (F) in a major inferotemporal retinal artery of the left eye at baseline with the subjects seated, during a 30 minute period with subjects lying on their right side, and during the following 20 minute period with subjects once again seated. A vital signs monitor was used to record the pulse rate and the brachial artery blood pressure. Retinal perfusion pressure (PP) was calculated according to the method of Hague and Hill (Br J Ophthalmol 1988;72:253–7). We studied ten women, ages 40 to 60, with NTG, four treated with Alphagan (brimonidine tartrate) and six with Xalatan (latanoprost ophthalmic solution). We compared the results to those from an age–matched control group of six healthy women. Results: In contrast to the control group where the magnitude of the change in F while recumbent was 7±6% (mean±sd) in response to an increase in PP of 39±18%, the NTG patients treated with Xalatan exhibited either large increases or large decreases in F while recumbent or while re–seated following recumbency. In these patients, the change in F while recumbent was 44±25%, while PP increased by 32±17%. Interestingly, in the NTG patients treated with Alphagan, F remained quite steady during and following recumbency. The change in F while recumbent was 11±11%, while PP increased by 32±28%. ANOVA showed significant (p=0.004, seated to recumbent; p=0.017, recumbent to re–seated) treatment effects on the change in F. Post hoc comparisons showed significant differences between the Xalatan group versus the control and Alphagan groups. Conclusions: In experimental studies, Alphagan treatment has been shown to be neuroprotective, maintaining the viability of retinal ganglion cells in the face of ischemia–reperfusion injury. Our preliminary study suggests that Alphagan, unlike Xalatan, acts to preserve retinal blood flow homeostasis during changes in perfusion pressure in NTG patients.
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