CORRECTION OF HYPERTENSIVE NEURORETINOPATHY BY DIMETHYLAMINOETHANOL DERIVATIVE 7-16 IN EXPERIMENT

Aim. Increase of efficiency of pharmacological correction of hypertensive neuroretinopathy using a new dimethylaminoethanol (DMAE) derivative 7-16.

Materials and methods. Modeling of hypertensive neuroretinopathy was carried out by introducing a nonselective inhibitor of NO-synthase N-nitro-L-arginine-methyl ester in a dose 12.5 mg/kg within 28 days and increasing intraocular pressure to 110 mm Hg by exerting mechanical pressure on the anterior chamber of the eye. To study the fundus of experimental animals, direct ophthalmoscopy (ophthalmoscope Bx a Neitz, Japan) was used. To zoom a lens Osher MaxField 78D model OI-78M has been used. Electroretinography was performed immediately after ophthalmoscopy. The ERG was recorded in response to a single stimulation. The induced biopotentials were amplified, averaged and presented graphically on the screen with the help of Biopac-systems MP-150 with the program AcqKnowledge 4.2 (USA). To assess the degree of development of functional damage to the retina, the ratio of the amplitudes of the b- and a-waves of the ERG, the coefficient b/a, was estimated.

Results. The expressed protective properties of the DMAE derivative 7-16 in a dose 25 mg/kg/day, exceeding its effect in a dose 12.5 mg/kg/day, were found, which resulted in a decrease of development of neuronal damage and vascular changes in the retina on the background of hypertension, which were noted in control group; an increase in the coefficient b/a in groups with the correction of pathology, which is caused by the restoration of the positive wave b on the ERG and indicates the preservation of the electrophysiological function of the bipolar and Müllerian cells.

Conclusion. The search of new ways to reduce the damaging effect of ischemia formed in hypertensive neuroretinopathy in the experiment is a vital task of pharmacology, which can be solved by using a new DMAE derivative 7-16.