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S. Shukhaev, A. Varavka; Atropine Does Not Contribute Into the Intraocular Pressure–Controlling Effect of Latanoprost . Invest. Ophthalmol. Vis. Sci. 2006;47(13):400.
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To study the influence of atropine on hypotensive effect caused by administration of latanoprost.
This randomized double–masked study included 20 patients, 7 male and 13 female, from 49 to 82 years of age. All patients had senile cataract. Experiment included a series of intraocular pressure (IOP) measurements. Baseline IOP was measured once, at 10 a.m. Then, at 3 a.m. of the next day, 1 drop of latanoprost (0,005%) was topically administered in patients’ one eye and 1 drop of placebo was topically administered in the fellow eye. Then, between 10 a.m. and 4 p.m. of the same day, 1 drop of 1% solution of atropine–sulfat was administered hourly, only in 1 eye, and IOP difference was measured with pneumatonometry every hour, also from 10 a.m. to 4 p.m.
Latanoprost caused significant decrease of the IOP, with peak effect in 10 hours after the administration, with average reduction by 6.08±0.2mmHg (35%, p=0.05), as compared with both the baseline IOP and the placebo effect. The mean difference in IOP reduction between latanoprost and placebo was 3.0±0,5mmHg (p=0,041). Atropine did not appear to have any influence onto intraocular pressure either combined with latanoprost, or as a monotherapy, as compared with either latanoprost in monotherapy or placebo. IOP alteration differences were statistically insignificant (p>0,05).
Relaxation of ciliary muscle supposedly leads to the increase of uveoscleral outflow. However, our study has shown that pronounced relaxation of ciliary muscle did not influence the efficacy of latanoprost. Thus, we suppose that ciliary muscle tonus does not affect the efficacy of latanoprost therapy.
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