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Background: Prostaglandin F(2alpha) analogues are effective intraocular-pressure-lowering drugs. Dietary fatty acids affect endogenous prostaglandin F(2alpha) concentrations and may thus influence intraocular pressure., Objective: We prospectively examined dietary fat consumption in relation to primary open-angle glaucoma (POAG)., Design: Women (n = 76 199 in the Nurses' Health Study) and men (n = 40 306 in the Health Professionals Follow-Up Study) free of POAG in 1980 and 1986, respectively, were followed until 1996 if they were > or =40 y old and reported receiving eye exams during follow-up. Potential confounders were assessed on biennial questionnaires, and energy-adjusted cumulative averaged fat intakes were measured by using validated food-frequency questionnaires. We analyzed 474 self-reported POAG cases confirmed by medical chart review. Cohort-specific multivariate rate ratios (RRs) were obtained by using proportional hazards models and were then pooled., Results: Major fats and fat subtypes were not independently associated with POAG risk. Pooled multivariate RRs (95% CI) for POAG comparing the highest with the lowest quintile of fat intake were as follows: 0.90 (0.67, 1.21) for total fat, 1.03 (0.77, 1.38) for saturated fat, 0.76 (0.56, 1.03) for monounsaturated fat, and 0.87 (0.66, 1.16) for polyunsaturated fat, none of which were statistically significant. We found a suggestive positive association between a higher ratio of n-3 to n-6 polyunsaturated fat and risk of POAG [RR = 1.49 (1.11, 2.01); P for trend = 0.10], which was stronger for high-tension POAG [RR = 1.68 (1.18, 2.39); P for trend = 0.009]., Conclusion: A high ratio of n-3 to n-6 polyunsaturated fat appears to increase the risk of POAG, particularly high-tension POAG. Further studies are needed.

Objective: To examine the association between cigarette smoking and incident primary open-angle glaucoma (POAG)., Methods: Female nurses and male health professionals were prospectively followed up from 1980 and 1986, respectively, to 1996. Participants were at least 40 years old, were free of diagnosed glaucoma at baseline, and reported being examined by an ophthalmologist or optometrist during follow-up. Smoking history and other POAG risk factors were updated with biennial questionnaires. A total of 450 incident cases of POAG were identified. Both cohort-specific proportional hazards analyses and analyses pooled across cohorts were conducted., Results: After controlling for potential risk factors of POAG, including age, hypertension, and African American heritage, neither current smokers (relative risk, 0.85; 95% confidence interval, 0.62-1.18) nor past smokers (relative risk, 0.91; 95% confidence interval, 0.63-1.32) were at greater risk for POAG than those who had never smoked. Heavier smoking did not increase the risk of POAG. A modest inverse association was observed with pack-years of smoking: those with 30 or more pack-years had a 22% reduced risk of POAG (relative risk, 0.78; 95% confidence interval, 0.55-1.11; P for linear trend,.06) than those who had never smoked., Conclusion: Cigarette smoking is not an important risk factor for POAG.

The relation between dietary antioxidant intake and primary open-angle glaucoma risk was examined in participants aged over 40 years in the Nurses' Health Study (n = 76,200) and the Health Professionals Follow-up Study (n = 40,284). They were followed biennially from 1980 and 1986, respectively, to 1996, during periods when they received an eye examination. Dietary intakes were measured repeatedly from 1980 in the Nurses' Health Study and from 1986 in the Health Professionals Follow-up Study using validated food frequency questionnaires. The authors analyzed 474 self-reported glaucoma cases confirmed by medical chart review to have primary open-angle glaucoma with visual field loss. The authors used Cox proportional hazards models for cohort-specific multivariate analyses, and results were pooled using random effects models. The pooled multivariate rate ratios for primary open-angle glaucoma comparing the highest versus lowest quintile of cumulative updated intake were 1.17 (95% confidence interval (CI): 0.87, 1.58) for alpha-carotene, 1.10 (95% CI: 0.82, 1.48) for beta-carotene, 0.95 (95% CI: 0.70, 1.29) for beta-cryptoxanthin, 0.82 (95% CI: 0.60, 1.12) for lycopene, 0.92 (95% CI: 0.69, 1.24) for lutein/zeaxanthin, 1.05 (95% CI: 0.59, 1.89) for vitamin C, 0.97 (95% CI: 0.62, 1.52) for vitamin E, and 1.11 (95% CI: 0.82, 1.51) for vitamin A. In conclusion, the authors did not observe any strong associations between antioxidant consumption and the risk of primary open-angle glaucoma.

Temporary retinal ischemia in the rat leads to a proliferation of endothelial cells and glial cells. We tested the hypothesis that this proliferation is caused by a release of soluble mitogens from the ischemic retina. Conditioned media were prepared from normal rat retina and from retina that had undergone 2 h ischemia and 48 h reperfusion, at which time it showed intense mitotic activity. The conditioned media were placed in cultures of fibroblasts, bovine adrenal capillary endothelial cells, and rat brain astrocytes. Cell proliferation in vitro was stimulated by the retinal extracts in all cell cultures. However, the cell proliferation in cultures with conditioned media from normal retina was similar to that in cultures with conditioned media from ischemic and proliferating retina. Although these data are consistent with the presence of soluble growth factors in the retina, they also indicate that release of these growth factors into the surrounding milieu after transient retinal ischemia is not altered to a degree that would explain the dramatic increase in mitosis.

We developed a quantitative histologic method for assessing injury in the rat retina due to transient ischemia. We used this technique to test the effectiveness of local hypothermia and allopurinol, an inhibitor of oxygen-free radical formation, in reducing ischemia/reperfusion injury in the rat retina. Retinal ischemia and reperfusion was produced by transient ligation of the optic nerve. Histologic evaluation by a masked observer was based on the average count of nonpyknotic nuclei in the inner nuclear layer of the retina from eight high power fields (X100) in one 5 microns thick sagital section at or near the optic nerve. A sharp increase in tissue damage occurs between 90 and 120 min of ischemia. Ischemia for periods of 60 and 90 min produced mild damage while periods of 120 and 240 min produced severe damage. Hypothermia protected the retina significantly from 120 min of ischemic injury (P less than 0.001 student t-test, compared to 120 min control), while allopurinol had no protective effect.