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PS Kulkarni, J Cai, HE Hurst; Fatty Acids, Nitric Oxide And Pig Retinal Circulation . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1972.
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Purpose: To determine the role of lipids and nitric oxide (NO) in the pig retinal and choroidal vessels. Methods: The lipid profiles of pig retina, and retinal and choroidal vessels were analyzed using GS/MS spectrometry; while the release of prostaglandins (PGs) and NO was determined in the perfused pig retinal arterioles. Results:The retina and both isolated retinal and choroidal vessels contained saturated fatty acid stearic acid and polyunsaturated fatty acids, including arachidonic (C20:4, AA), a precursor for vasoactive prostaglandin (PG-2) series, and W-6 docosahexaenoic acids (C22:6, DHA). The retina contained relatively higher amounts of DHA than AA, retinal vessels had equal amounts of AA and DHA, while choroidal vessels contained higher amounts of AA than DHA. We also examined the endogenous synthesis/release of vasoactive PGs and NO in the pig retinal vessels. Since angiotensin II (Ang II) releases these products from blood vessels, this polypeptide was used. The pig retinal central artery was perfused with oxygenated/heparinized physiological salt solution at 37°C. Changes in A1 and A2 arteriolar diameters induced by Ang II were determined in the absence and presence of NO synthase inhibitor, l-NO Arginine (LNOA), and cyclooxygenase inhibitor, flurbiprofen (FB). The central retinal artery designated as the first order arteriole A1 and subsequent branch was defined as A2. Luminal diameters of A1 and A2 arterioles were 35 ± 2 mm and 10 ± 1 mm, respectively. Topical Ang II (10-10 M - 10-6 M) caused small vasoconstrictions in a dose-dependent manner. This response was enhanced after inhibition of PG synthesis by (10-6 M) FB. Ang II induced-constrictions were further enhanced in the presence of NO synthase inhibitor, LNOA (10-7 M). There was slightly more increase in Ang II-induced vasoconstrictions in the presence of both NO and PG inhibitors, suggesting that NO may cause release of PGs from these vessels. Conclusion: This study demonstrates that the endogenous vasodilating PGs and NO, (especially NO), may play a vital role locally in pig retinal circulation.
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