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The effects of exercise on intraocular pressure in pigmentary glaucoma patients.

Previous studies of normal volunteers and open-angle glaucoma patients have shown that exercise temporarily lowers intraocular pressure. However, two case reports have described pigmentary dispersion syndrome patients who developed symptomatic increased intraocular pressure after exercise. We evaluated the intraocular pressure response to exercise in ten pigmentary glaucoma patients. An exercise protocol was designed to increase the likelihood of lens zonule-iris pigment epithelium contact. Intraocular pressure measurements during the first two hours after exercise showed no statistically significant elevation of mean intraocular pressure. The pressure rose 6 mm Hg and 7 mm Hg respectively at 15 minutes in two eyes, but returned to baseline by 30 minutes. Our results suggest that exercise may not significantly increase the clinical intraocular pressure in pigmentary glaucoma patients.

Adult↗

The effect of dopamine on the intraocular pressure and pupil of the rabbit eye.

The presence of a dopamine-specific receptor that can influence intraocular pressure in the rabbit eye is suggested by these experiments: intravitreal, systemic, or topically administered dopamine solutions can produce a decrease in intraocular pressure that is dose-dependent. In high doses the decrease in intraocular pressure is accompanied by mydriasis, and alpha-adrenergic pupillary response. This alpha-response may be caused by dopamine as a direct, but weak alpha-stimulator or by displacement of norepinephrine onto the receptor from its storage site. At lower doses the decrease in intraocular pressure occurs in the absence of mydriasis and in spite of blockade of beta-adrenergic receptors. Further, a specific dopaminergic blocker, haloperidol, prevents this decrease in intraocular pressure. The decreases are small, but reproducible and suggest that dopamine can influence the adrenergic regulation of intraocular pressure.

Administration, Topical↗

Intraocular pressure and proptosis in 95 patients with Graves ophthalmopathy.

PURPOSE: To study the cause of ocular hypertension in patients with Graves ophthalmopathy. METHODS: Intraocular pressure was measured in 190 eyes of 95 patients (mean age, 42 years; range, 11 to 86 years) with Graves ophthalmopathy. In six eyes (four patients), changes in intraocular pressure were also analyzed upon orbital decompression. RESULTS: The mean intraocular pressure +/- SD in 190 eyes was 18.36 +/- 4.02 mm Hg (range, 10 to 34 mm Hg). The intraocular pressure in 42 of the 190 eyes was 21 mm Hg or more. The intraocular pressure in 76 eyes with proptosis of 19 mm or more was 19.96 +/- 4.49 mm Hg (range, 14 to 34 mm Hg), whereas the intraocular pressure in 114 eyes with proptosis of less than 19 mm was 17.08 +/- 3.38 mm Hg (range, 10 to 28 mm Hg). The difference in the values between these two groups is statistically significant (two-tailed t test, P < .001). The mean intraocular pressure in six eyes decreased from 23.23 to 18.82 mm Hg upon orbital decompression, a difference that was statistically significant (two-tailed paired t test, P < .001). The coefficient of outflow facility was normal in these six eyes. CONCLUSION: These findings suggest that ocular hypertension in patients with Graves ophthalmopathy is caused, in part, by increased intraorbital pressure associated with proptosis.

Adolescent↗

Blood flow and glucose consumption in the optic nerve, retina and brain: effects of high intraocular pressure.

Glucose consumption and regional blood flow were determined using the [14C]-2-deoxyglucose (2-DG) method and microspheres in the optic nerve, the retina and different parts of the brain in monkeys. The relationship between the 2-DG accumulation and blood flow in the optic nerve head region was similar to that in grey matter of the brain under pentobarbital anaesthesia as well as under urethan anaesthesia. Pentobarbital anaesthesia resulted in lower values for blood flow and glucose metabolism in most regions. In the optic nerve the highest values were observed in the distal part; there was a fall in blood flow and metabolism along the nerve. There was a corresponding increase in myelin content. Artificial increments in intraocular pressure resulting in a perfusion pressure (mean arterial pressure minus intraocular pressure) of 40 cm H2O had no appreciable effect on the 2-DG accumulation. At a perfusion pressure of 20 cm H2O 2-DG accumulation in the retina and prelaminar part of the optic nerve was markedly increased indicating partial ischemia resulting in anaerobic glycolysis. At intraocular pressures higher than the systolic arterial blood pressure there was still some accumulation of 2-DG in the intraocular tissues, but no blood flow, which indicates that glucose could diffuse into the eye through the sclera. Behind the lamina cribrosa there was no indication of a reduction in blood flow or a metabolic disturbance. The results indicate that the blood flow and metabolism of the retina and prelaminar part of the optic nerve is disturbed only at very high intraocular pressures, and that even at extreme pressures there is no disturbance behind the lamina cribrosa in acute experiments. The 2-DG method will be useful in further studies on the nutritional status of the optic nerve head since it can detect abnormal glycolysis even in very discrete regions due to its high spatial resolution.

Animals↗

Intraocular pressure during hemodialysis.

In 14 patients undergoing hemodialysis, the intraocular pressure did not change significantly when measured at hourly intervals for 4 h. There was a loss in body weight because of fluid loss; also the Schirmer values decreased significantly at the conclusion of treatment. Blood osmolality decreased markedly in a linear fashion. The fluctuations of intraocular pressure during hemodialysis were likely dependent on the dynamics of dehydration and hypo-osmolality. Regulatory forces stabilized the intraocular pressure to such a degree that statistical significance in these fluctuations was not reached.

Adult↗