title: Effect of CO(2) pneumoperitoneum on early cellular markers of retinal ischemia in rabbits with alpha-chymotrypsin-induced glaucoma.
abstract: 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 CO(2) 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 CO(2) pneumoperitoneum, or (c) a 20 mmHg CO(2) 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.
  
  
  CONCLUSIONS
  In rabbits with alpha-chymotrypsin-induced glaucoma, a 4-h CO(2) pneumoperitoneum of </=20 mmHg in the head-down position did not induce either retinal layer disorganization or alteration of actin or vimentin.
authors: Department of Anesthesia, Université Paris-Sud, Hôpital Antoine Béclère, 157 rue de la Porte de Trivaux, 92141 Clamart Cedex, France.
authors: C
authors: C
authors: Lentschener
authors: D
authors: D
authors: Fredi-Reygrobellet
authors: H
authors: H
authors: Bouaziz
authors: J X
authors: JX
authors: Mazoit
authors: F
authors: F
authors: Niessen
authors: D
authors: D
authors: Benhamou
mesh_terms: D000199:Actins / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D015415:Biomarkers; D002245:Carbon Dioxide; D002918:Chymotrypsin; D005901:Glaucoma / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D018475:Head-Down Tilt / Q000009:adverse effects; D007150:Immunohistochemistry; D007429:Intraocular Pressure / Q000502:physiology; D007511:Ischemia / Q000378:metabolism / Q000503:physiopathology*; D011028:Pneumoperitoneum, Artificial / Q000009:adverse effects* / Q000379:methods; D011817:Rabbits; D011897:Random Allocation; D012160:Retina / Q000378:metabolism; D012171:Retinal Vessels / Q000378:metabolism*; D013997:Time Factors; D014746:Vimentin / Q000378:metabolism
chemical_list: D000199:Actins; D015415:Biomarkers; D014746:Vimentin; D002245:Carbon Dioxide; D002918:Chymotrypsin; C117608:alpha-chymotrypsin