Effect of CO2 pneumoperitoneum on early cellular markers of retinal ischemia in rabbits with α-chymotrypsin-induced glaucoma

Background: Increased intraperitoneal pressure in the head-down position is associated with a significant increase in intraocular pressure (IOP) in rabbits with alpha -chymotrypsin-induced glaucoma. Also, the retinal cells are weakened by the induction of increased IOP, and/or glaucoma, even when IOP is controlled by adequate therapy; therefore, these cells need to be protected from any additional aggression. Actin and vimentin are proteins of the retinal cell cytoskeleton that react readily in response to retinal injuries, including ischemia and glaucoma. Early changes in these cytoskeleton proteins determine the morphological changes observed after retinal damage. Therefore, we set out to investigate intracytoplasmic changes in vimentin and actin after a 4-h CO2 pneumoperitoneum in the head-down position in rabbits with alpha -chymotrypsin-induced glaucoma. Methods: Twenty-one rabbits with alpha -chymotrypsin-induced glaucoma in one eye received general anesthesia for 4 h in the head-down position and were randomly allocated to have (a) no pneumoperitoneum, (b) a 10 mmHg CO2 pneumoperitoneum, or (c) a 20 mmHg CO2 pneumoperitoneum. At the end of the trial, both the right glaucomatous and the left control eyes were enucleated and investigated immunocytochemically for alterations in vimentin and actin, and morphologically for retinal layer disorganization. Results: Except for the preexisting morphological changes induced by glaucoma, both the control and the glaucomatous eyes in all rabbits appeared normal in terms of retinal layer organization and the distribution of intracellular vimentin and actin whatever the intraperitoneal pressure level applied. Conclusion: In rabbits with alpha -chymotrypsin-induced glaucoma, a 4-h CO2 pneumoperitoneum of less than or equal to 20 mmHg in the head-down position did not induce either retinal layer disorganization or alteration of actin or vimentin.