Contact lens-induced edema in vitro--amelioration by lactate dehydrogenase inhibitors.
Isolated rabbit corneas bathed in Krebs-bicarbonate Ringer solution were observed for thickness changes after a 90 minute equilibration period. Control corneas swelled an average of 0.5 micron/hr, and placement of a polymethylmechacrylate (PMMA) contact lens on the epithelial surface caused the corneas to swell 24.5 microns/hr, an effect similar to 0.5 mM epithelial cyanide exposure. The pronounced swelling induced by PMMA lens placement was much less however, in the epithelial presence of 3.2 mM sodium oxalate (3.22 microns/hr) or 3.2 mM sodium oxamate (5.38 microns/hr). An equiosmotic excess of 4.8 mM NaCl was least active (15.89 microns/hr). On normal isolated corneas (without contact lenses), the Ringer containing an excess of 4.8 mM NaCl significantly deswelled the corneas (-13.44 microns/hr), which contrasted with oxalate and oxamate containing Ringer solutions (1.17 and 1.33 micron/hr respectively). The present study supports the notion that contact lens-induced edema results from stromal lactate accumulation, and suggests a potential alternative to osmotic therapy for its amelioration. These LDH inhibitors, in the concentrations used, have no acute osmotic or toxic effect on normal corneas in vitro.
D000596:Amino Acids / Q000627:therapeutic use*; D000818:Animals; D003261:Contact Lenses / Q000009:adverse effects*; D003316:Corneal Diseases / Q000188:drug therapy* / Q000209:etiology; D004487:Edema / Q000188:drug therapy* / Q000209:etiology; D005260:Female; D007770:L-Lactate Dehydrogenase / Q000037:antagonists & inhibitors*; D008297:Male; D010070:Oxalates / Q000627:therapeutic use*; D019815:Oxalic Acid; D010072:Oxamic Acid / Q000627:therapeutic use*; D011817:Rabbits
D000596:Amino Acids; D010070:Oxalates; D019815:Oxalic Acid; D007770:L-Lactate Dehydrogenase; D010072:Oxamic Acid