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Abstract #5628 Published in IGR 2-1
The significance of nitric oxide for parasympathetic vasodilation in the eye and other orbital tissues in the cat
Nilsson SFExperimental Eye Research 2000; 70:61-72
The role of nitric oxide formation in the vasodilation in the eye and other orbital tissues caused by pre-ganglionic stimulation of the facial nerve was studied in cats under alpha-chloralose anaesthesia. Regional blood flows were determined with radioactive microspheres during unilateral stimulation of the facial nerve before and after inhibition of nitric oxide synthase (NOS), alone or in combination with muscarinic blockade. N(omega)-nitro-L-arginine (L-NA), a non-selective NOS-inhibitor, caused a significant increase in mean arterial blood pressure (MABP) and a decrease in cardiac output (CO). Concomitantly, local blood flows on the non-stimulated control side were reduced in most of the investigated tissues, indicating marked vasoconstriction. An inhibitor selective for neuronal NOS, 7-nitro-indazole (7-NI), had no significant effect on MABP, CO or local blood flows. During facial nerve stimulation at 5 Hz (n=6), choroidal blood flow on the stimulated side was 108±41% (p < =0.05) higher than on the non-stimulated side during control conditions, an effect that was completely abolished by L-NA. During stimulation at 10 Hz (n=8), the choroidal blood flow was 171±38% (p < =0.01) higher on the stimulated side during control conditions. The corresponding values after L-NA and subsequent administration of atropine were 97±21% (p < =0.05, compared to control conditions) and 50±14% (p < =0.05, compared to control conditions), respectively. Atropine alone had no significant effect on the increase in choroidal blood flow caused by stimulation at 10 Hz (n=7), whereas subsequent administration of L-NA caused a statistically significant reduction. Administration of 7-NI had no significant effect on the choroidal vasodilation at 10 Hz (n=7), whereas subsequent administration of L-NA caused significant reduction, at least as compared to control conditions. These results suggest that nitric oxide is of greater significance for the choroidal vasodilation, caused by facial nerve stimulation, in the cat than it is in the rabbit. However, no definitive conclusions can be made concerning the source of the nitric oxide. Direct release of nitric oxide from the parasympathetic nerve fibers could contribute as well as nitric oxide formed in the vascular endothelium, secondary to the release of acetylcholine and/or VIP. At high frequencies, a part of the choroidal vasodilation seems to be independent of nitric oxide.
Dr. S.F. Nilsson, Department of Physiology, University of Uppsala, Uppsala, Sweden SivNi@imv.liu.se
Classification:
5 Experimental glaucoma; animal models
6.11 Bloodflow measurements (Part of: 6 Clinical examination methods)