September 1996
Volume 37, Issue 10
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Articles  |   September 1996
Nitric oxide as a mediator of parasympathetic vasodilation in ocular and extraocular tissues in the rabbit.
Author Affiliations
  • S F Nilsson
    Department of Physiology and Medical Biophysics, University of Uppsala, Sweden.
Investigative Ophthalmology & Visual Science September 1996, Vol.37, 2110-2119. doi:
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      S F Nilsson; Nitric oxide as a mediator of parasympathetic vasodilation in ocular and extraocular tissues in the rabbit.. Invest. Ophthalmol. Vis. Sci. 1996;37(10):2110-2119.

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Abstract

PURPOSE: The aim of this study was to investigate in rabbits the relationship between nitric oxide and the noncholinergic vasodilation caused by facial nerve stimulation in the eye and some extraocular tissues. METHODS: Uveal vascular resistance was determined by measuring simultaneously the flow from a cannulated vortex vein with intraocular pressure and arterial blood pressure recordings. The local blood flow in different parts of the eye (iris, ciliary body, choroid, and retina), eyelids, nictitating membrane, Harderian gland, and lacrimal gland was determined using radioactive microspheres. The effects of facial nerve stimulation, at different frequencies, were examined before and after the administration of nitric oxide synthase (NOS) inhibitors. RESULTS: In the experiments with direct determination of uveal blood flow, stimulation of the facial nerve caused a frequency-dependent decrease in uveal vascular resistance, indicating vasodilation. This effect was reduced or abolished by NOS inhibition at low frequencies but was unaffected at high frequencies. Determination of regional blood flow, with radioactive microspheres, showed that the stimulation increased local blood flow in all parts of the uvea. Compared to the nonstimulated control side, stimulation at 2 Hz increased choroidal blood flow by 89% +/- 12% before NOS inhibition and by 45% +/- 10% after NOS inhibition, a difference of 44% +/- 77% (n = 9; P < or = 0.05). Iris and ciliary body vasodilation appeared to be equally reduced. In eyelids, Harderian gland, and lacrimal gland, the vasodilation elicited by stimulation at 2 Hz was abolished almost completely by NOS inhibition. The vasodilation in most of the extraocular tissues was reduced significantly by NOS inhibition at 5 Hz, with only a slight reduction in the choroid, iris, and ciliary body. Retinal blood flow also was significantly increased by facial nerve stimulation at 2 Hz and 5 Hz. The increase in retinal blood flow appeared to be more sensitive to NOS inhibition than the increase in uveal blood flow. CONCLUSIONS: These results suggest that the formation of nitric oxide plays an important role in the uveal, retinal, and extraocular vasodilation brought about by facial nerve stimulation at low frequencies. At high frequencies, other neurotransmitters also seem to be involved.

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