Original articleA Rat Model for Acute Rise in Intraocular Pressure: Immune Modulation as a Therapeutic Strategy
Section snippets
Animals
Inbred adult male Lewis rats (average weight 250 g, age eight weeks) were supplied by the Animal Breeding Center at the Weizmann Institute of Science. The rats were raised in a light- and temperature-controlled room and were matched for age and weight before each experiment. All animals were handled according to the regulations formulated by the International Animal Care and Use Committee (IACUC) and the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research. Institutional
Induction of an acute increase in intraocular pressure in rats
Saline infusion to the rats’ anterior chamber caused IOP rise to 100 cm H2O; this was equal to the height of the infusion bag. Twenty-four hours after elevation, the mean IOP had returned to normal (19 ± 4 mm Hg).
Loss of retinal ganglion cells caused by acute increase in intraocular pressure
To investigate the effect of IOP on RGC survival we examined three groups of rats. Rats in group 1 (n = 6), which served as a control, were not subjected to an increase in IOP. Rats in group 2 (n = 14) and group 3 (n = 12) were subjected for one hour to an IOP insult, as described
Discussion
In the rat model of acute rise in IOP described here, the increase in pressure was controlled, transient, and reproducible. Since there was no evidence of other damage in these eyes, the loss of RGCs can be assumed to be caused solely by the acute increase in IOP; loss of RGCs is amenable to neuroprotective therapy.
An acute increase in IOP in the eyes of experimental animals can also be induced by pharmacological and surgical interventions.2, 3, 4, 5, 6, 7, 28 All of these methods, however, are
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The authors thank Michal Schwartz, PhD, and Larry Wheeler, PhD, for their assistance in study design, analyzing and interpreting the results, and critical review of the manuscript.