Ophthalmic research
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Ophthalmic research · Jan 2011
Effects of propofol and isoflurane anesthesia on the intraocular pressure and hemodynamics of pigs.
To determine the conditions under which anesthetized pigs can be used in acute noninvasive investigations of ocular hydro- and hemodynamics, the intraocular pressure (IOP) of adult pigs was recorded under the following conditions: (1) after intravenous injection of propofol plus ketamine; (2) during inhalation of isoflurane, and (3) 2 h after topical administration of bimatoprost or (4) timolol. Propofol/ketamine and isoflurane induced significant decreases in the IOP. The pulsation of the ophthalmic artery appeared at a significantly higher IOP in animals anesthetized with isoflurane than in those anesthetized with propofol/ketamine. ⋯ It is concluded that different techniques for the acute noninvasive investigation of ocular hydro- and hemodynamics are applicable in anesthetized pigs. To test the effects of antiglaucoma agents, investigation periods longer than 2 h are required. We recommend the use of intravenous propofol/ketamine anesthesia rather than isoflurane anesthesia in future experiments using pigs.
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Ophthalmic research · Jan 2009
JNK MAPK signaling contributes in vivo to injury-induced corneal epithelial migration.
Injury-mediated corneal epithelial wound healing in vivo is mediated through different cell signaling pathways depending on whether or not the basement membrane is removed. Given this dependence, we ascertained if c-jun N-terminal kinase (JNK/SAPK) mitogen-activated protein kinase (MAPK) cell signaling mediates this response in vivo and in vitro, irrespective of the presence or absence of the basement membrane. Furthermore, in vitro the relative contribution was determined by the JNK/SAPK pathway to that of its p38 and ERK MAPK counterparts in mediating injury-induced increases in cell migration. ⋯ JNK/SAPK pathway activation stimulates wound healing in vitro and in vivo, irrespective of the presence or absence of the basement membrane. Therefore, studies on how wound closure is elicited in HCEC are relevant for identifying how MAPK signaling mediates this response in vivo and in organ-cultured eyes. This realization suggests that the JNK signaling system has a role in vivo that is intermediate to those of ERK and p38 in mediating increases in cell migration.
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Advanced glycation end products (AGEs) play an important role in protein modification during cataract formation. Along with sugars, alpha-dicarbonyl compounds, such as methylglyoxal (MGO), have been implicated in AGE formation. Here we report the effect of pyridoxamine (PM) on AGEs and AGE-precursor-metabolizing enzymes in diabetic rat lenses and organ-cultured rat lenses. ⋯ Our results suggest that PM can inhibit AGE formation in the diabetic lens by enhancing the activity of aldose reductase and reacting with precursors of AGEs.
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Ophthalmic research · Sep 2005
Effect of alpha-melanocyte-stimulating hormone on interleukin 8 and monocyte chemotactic protein 1 expression in a human retinal pigment epithelial cell line.
To examine melanocortin receptor (from MC-1 to MC-5) mRNA and the effect of alpha-melanocyte-stimulating hormone (alpha-MSH) on interleukin 8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) expression in a human retinal pigment epithelial cell line (ARPE-19) stimulated with IL-1beta or tumor necrosis factor alpha (TNF-alpha). ⋯ ARPE-19 cells had MC-1 mRNA. alpha-MSH inhibited IL-8 and MCP-1 expression and protein secretion. Possibly, the effect on chemotactic factors may be via suppression of NF-kappaB translocation.
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Ten years ago a 45-year-old female presented with bilateral maculopathy with visual acuity of 6/18 on the right and 6/24 on the left. She had been on fluphenazine for the past 10 years for schizophrenia. ⋯ A previous publication has reported maculopathy with fluphenazine in association with the welding arc injury, but that particular patient had not been exposed to welding flash or other extreme photochemical sources. We believe this is the first reported incidence that fluphenazine has directly caused a maculopathy secondary to its accumulation at the retinal pigment epithelium and its toxic effect.