Zusammenfassung
Objective To examine structural changes and aqueous humor outflow after viscocanalostomyin live normal monkey eyes.
Methods Viscocanalostomy surgery was performed in 1 eye of each of 4 rhesusmonkeys. Outflow facility was determined before and after surgery. All eyeswere fixed and examined by light and/or electron microscopy 36 or 63 dayspostoperatively.
Results Schlemm canal was replaced ...
Zusammenfassung
Objective To examine structural changes and aqueous humor outflow after viscocanalostomyin live normal monkey eyes.
Methods Viscocanalostomy surgery was performed in 1 eye of each of 4 rhesusmonkeys. Outflow facility was determined before and after surgery. All eyeswere fixed and examined by light and/or electron microscopy 36 or 63 dayspostoperatively.
Results Schlemm canal was replaced by scar tissue at the surgical site. Thejuxtacanalicular zone contained homogeneous material, probably high-molecular-weight1.4% sodium hyaluronate. The sclera external to Schlemm canal was overhydrated,and remains of a scleral lake were present in 1 animal. Multiple defects werepresent in the endothelial lining of Schlemm canal inner and outer wall. Finefibrillar material and sheath-derived plaque material partly bridged the defects.Along the inner wall, aggregations of thrombocytes covered some defects inthe endothelial lining of the canal. At 90° to 180° from the surgicalsite, small and fewer breaks in the inner wall were seen. Postsurgery outflowfacility (n = 2) was approximately 30% higher in the treated eyethan in the contralateral control, corrected bilaterally for presurgery baseline.
Conclusions The most likely explanations for the increase in outflow facility inmonkeys after viscocanalostomy are focal disruptions of the inner wall endotheliumof Schlemm canal and disorganization of the juxtacanalicular zone, resultingin direct communication of juxtacanalicular zone extracellular spaces withthe lumen of Schlemm canal. The continuous presence of sodium hyaluronatemight prevent repair of these defects by interfering with thrombocyte function.
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