Differential effects of nitric oxide and cyclo-oxygenase inhibition on the diameter of porcine retinal vessels with different caliber during hypoxia ex vivo. (July 2017)

• Record Type: Journal Article
• Authors: Skov Jensen, Peter; Aalkjaer, Christian; Bek, Toke
• Is Part Of: Experimental eye research. Volume 160(2017)
• Page Start: 38
• Page End: 44
• Publication Date: 2017-07
• Subjects: Retinal vessels -- Diameter regulation -- Ex vivo model -- Hypoxia -- Nitric oxide -- Cyclo-oxygenase; Ophthalmology -- Periodicals; Eye -- Periodicals; Œil -- Périodiques; Ophthalmology; Periodicals; Electronic journals; 612.8405
• DOI: 10.1016/j.exer.2017.04.001
• Languages: English
• ISSNs: 0014-4835

Abstract

Abstract: Background: Hypoxia induced relaxation of larger retinal arterioles has been shown to be mediated by nitric oxide (NO) and cyclo-oxygenase (COX) products both in vivo and in vitro. However, the involvement of smaller retinal vessels in the response is unknown. Therefore, the purpose of the present study was to investigate the effect of blocking the synthesis of NO and COX on hypoxia induced changes in the diameter of smaller porcine retinal vessels at different branching level. Methods: Porcine hemiretinas were mounted in a tissue chamber and were constricted with the prostaglandin agonist U46619. Changes in the diameter of arterioles, pre-capillary arterioles and capillaries were studied during hypoxia, in the presence of the COX inhibitor ibuprofen and the NO synthase inhibitor L-NAME. Results: In the presence of L-NAME hypoxia induced dilatation was significantly smaller in arterioles and capillaries than in precapillary arterioles (p < 0.04), whereas in the presence of ibuprofen the dilatation was significantly smaller in capillaries and pre-capillary arterioles than in arterioles (p < 0.04). Conclusions: The mechanisms underlying hypoxia induced dilatation differ among smaller porcine retinal vessels with different caliber ex vivo. This may reflect differences in the responses of retinal vessels to changes in metabolism, and may point to possible targets for pharmacological intervention on the diameter of retinal vessels with different caliber in vivo. Highlights: Hypoxia induced dilatation depends on the branching level of retinal vessels ex vivo. Nitric oxide and prostaglandins modify hypoxia induced dilatation of retinal vessels. Precapillary arterioles may be targets for intervention on retinal vascular disease.