Elimination of sodium hyaluronate-induced decrease in outflow facility with hyaluronidase.
The use of intraocular sodium hyaluronate is complicated by a postoperative rise in intraocular pressure (IOP). The rise in IOP is thought to stem from a "clogging" at the trabecular meshwork by the large molecules of hyaluronate. This study uses serial tonographic measurements in an animal model to document this change in outflow facility. Furthermore, we investigate the ability of the enzyme hyaluronidase to cleave the hyaluronate into smaller molecular weight fragments, in vivo, and thereby eliminate the change in outflow facility. This report demonstrates the potential usefulness of this enzyme and documents the lack of harmful side effects histopathologically.
D000818:Animals; D004195:Disease Models, Animal; D006820:Hyaluronic Acid / Q000009:adverse effects*; D006821:Hyaluronoglucosaminidase / Q000627:therapeutic use*; D007429:Intraocular Pressure / Q000187:drug effects; D008970:Molecular Weight; D011817:Rabbits; D014065:Tonometry, Ocular; D014129:Trabecular Meshwork / Q000187:drug effects*
D006820:Hyaluronic Acid; D006821:Hyaluronoglucosaminidase