Experimental ocular hypertension can be induced by production of a permanent condition of vascular stasis and congestion (ligating the vortex or ciliary veins), or by blockage of the circulation of the intraocular fluid after injecting nondiffusible oils, or by exciting inflammatory and proliferative reactions in the anterior chamber (Duke-Elder, 1940).1 More recently the discovery of sanguinarine poisoning as the cause of epidemic dropsy and its accompanying raised intraocular tension gave rise to new possibilities for studying glaucoma in the laboratory. Hakim2 (1954), and Leach and Lloyd3,4 (1955 and 1956), produced a raised intraocular pressure by administering argemone oil, which consists of sanguinarine and other allied alkaloids. While Leach and Lloyd were working on sanguinarine poisoning, they found that the control monkeys, which were getting an orange twice a week along with a stock diet, showed histopathological changes in the trabecular meshwork similar to that of the
RODGER FC, GROVER AD, SAIDUZZAFAR H. The Effect of Citral on Intraocular Dynamics in Monkeys. AMA Arch Ophthalmol. 1960;63(1):77–83. doi:10.1001/archopht.1960.00950020079012
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