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C. Zawinka, J. Kolodjaschna, L. Schmetterer, H.A. Reitsamer; Effect of NOS-1 Inhibition on Choroidal Blood Flow in Anesthetized Rabbits . Invest. Ophthalmol. Vis. Sci. 2003;44(13):349.
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Purpose:It has been shown previously that non selective inhibition of nitric oxide synthase causes choroidal vasoconstriction and a reduction of choroidal blood flow in anesthetized rabbits (J.W. Kiel 1999, Exp Eye Res. 69(4):413-29). In the present study, we sought to determine the contribution of the neuronal nitric oxide synthase (NOS-1) to choroidal blood flow regulation. Methods:Anesthetized rabbits (n=7) were instrumented with an ear artery cannula to measure mean arterial pressure (MAP), and a vitreous cannula to measure IOP; hydraulic occluders were placed around the descending aorta and the inferior caval vein to manipulate choroidal perfusion pressure over a wide range. Choroidal blood flow was measured by laser Doppler flowmetry. A protocol with three subsequent measurements was performed in each animal - pressure flow relationships and baseline data were recorded (1) under control conditions, (2) in response to TRIM (20 mg/kg, i.v. infusion) and (3) in response to L-NAME (15 mg/kg, i.v. bolus injection). Results:NOS-1 inhibition with TRIM had no statistically significant effect on baseline parameters and pressure flow relationships of the choroid. However, L-NAME injection after TRIM application showed a substantial reduction of choroidal blood flow and IOP and an increase in MAP, perfusion pressure and vascular resistance. Baseline values under control and drug conditions are shown as means ± s.e. in the table. L-NAME also shifted the pressure flow relationship significantly downwards. Conclusions: Choroidal nitric oxide vasodilator tone in the anesthetized rabbit seems largely to be due the activity of endothelial nitric oxide synthase. View OriginalDownload SlideView OriginalDownload Slide
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