Abstract
Purpose :
To evaluate the effect of the G661R missense mutation in the ADAMTS10 gene on ocular pulse amplitude (OPA) in dogs.
Methods :
Animals studied included 39 glaucomatous and 14 unaffected control male and female dogs between the ages of 6 months and 12 years (median: 3.2 years). Dogs were sedated with butorphanol and midazolam and average of both right and left eye were measured. Intraocular pressure (IOP) was measured with the Icare® Tonovet rebound tonometer. The Reichert Model 30™ Pneumotonometer was used to measure OPA, deviation index, and pulsation rate. During each session, measurements were taken twice, once for acclimation to the probe and noise of the pneumotonometer, and a second time for actual data collection. Central corneal thickness (CCT) measurements were taken via Accutome® PachPen, and A-scan biometry assessed with DGH Technology Scanmate. Data analysis was conducted with ANOVA, ANCOVA and regression models.
Results :
Mutant dogs had a significantly lower OPA of 4.24 +/- 2.05 mmHg (mean +/- SD) compared to 6.54 +/- 2.83 mmHg of normal dogs (p=0.002). There was no significant age effect, and OPA was not correlated with any other parameters, including CCT. As expected, mutant dogs displayed a greater mean IOP of 25.04 +/- 8.04 mmHg compared to 15.25 +/- 3.59 mmHg of normal dogs.
Conclusions :
The lower OPA in ADAMTS10-mutant dogs corresponds to previously documented weaker and biochemically distinct posterior sclera. OPA measurement could be a valuable in vivo clinical tool to assess individuals’ scleral biomechanics, and therefore their susceptibility to IOP elevation.
This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.