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The goal of the presented research was to assess the influence of continuously administered fentanyl on the intraocular pressure, pupil size and aqueous tear production in dogs. A prospective, randomised, double “blind” clinical study was performed. Twenty-five non-painful dogs, 13 breeds, a body weight of 10.0 ± 5.4 kg (mean ± SD) and age of 6.5 ± 3.3 years, 12 males and 13 females with no ocular abnormalities were randomly allocated into two groups receiving an intravenous injection of saline (SAL) 0.3 ml/kg followed by an infusion 2 ml/kg/h or an intravenous injection of fentanyl (FEN) 0.005 mg/kg (diluted in 0.3 ml/kg) followed by an infusion 0.005 mg/kg/h (diluted in 2 ml/kg/h). The intraocular pressure (IOP), pupil size (PS), pulse rate (PR), respiratory frequency (f_R) and systolic and diastolic arterial pressures (SAP, DAP) were measured before (baseline) and at 2, 5, 10, 20 and 30 minutes after the premedication. The Schirmer Tear Test I (STT-I) was measured prior to and at 30 min after the premedication. The data were analysed by Bartlett’s, Anderson-Darling and Dunnett’s tests, the t-test and an analysis of variance (ANOVA) (P < 0.05). Relative to the baseline, in the fentanyl group, the PS was significantly decreased at all time points, the PR was significantly decreased at T₃₀ and the f_R was significantly decreased at T₅, T₁₀, T₂₀ and T₃₀. There were no other significant changes in the IOP, STT-I, SAP and DAP relative to the baseline. Compared to the control group, in the fentanyl group, the PS was significantly smaller at T₂, T₅, T₁₀, T₂₀ and T₃₀, the PR was significantly lower at T₂, T₂₀ and T₃₀ and the f_R was significantly higher at T₂₀. Within thirty minutes of a constant rate infusion of fentanyl in the healthy non-painful dogs, the intraocular pressure and aqueous tear production were not affected. However, the fentanyl significantly decreased pupil size. This fact should be considered, when planning analgesia where miosis is undesirable.

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No abstract

Decrease and loss of vision are extremely important problems, quite common conditions that lead to disability. The most common causes are ischemic optic neuropathy, diabetic retinopathy, and amblyopia. The pathogenesis of these disea­ses is characterized by neurodegeneration, loss of structure and function of neurons. Citicoline may be considered for neuroprotection as the drug of choice in these clinical situations. Citicoline has antioxidant and anti-inflammatory properties, it reduces lipid peroxidation and the formation of free radicals, has anti-apoptotic and membrane-protective effects. The drug has a neuromodulatory effect and also contributes to the pre­servation of sphingomyelin, which ensures signal transmission in nerve cells. In ischemic optic neuropathy, oral citicoline can reduce nerve fiber loss and improve retinal ganglion cell function and visual tract function. In diabetic retinopathy, citicoline prevents synapse loss and improves macular and retinal ganglion cell function. In amblyopia, citicoline stimulates the function of neurotransmitters and neuromodulators, including an increase in the activity of endogenous dopamine and, at the same time, an improvement in the vascular aspects of neurological function. Axobrex is a convenient oral form of citicoline. With oral administration, the bioavailability of citicoline exceeds 90 %, Axobrex is non-toxic and very well-tolerated. The dosage regimen of Axobrex is simple, which contributes to satisfactory patient adherence to treatment. The use of Axobrex in patients with ischemic optic neuropathy, diabetic retinopathy, and amblyopia has an optimal balance of benefits and safety and is advisable for neuroprotection.