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Monique Michelle McCallister, Jessica Kunkel, John M Scichilone, John Kuchtey, Rachel W Kuchtey; Calibration of TonoLab rebound tonometer is not affected by extremely thin corneas in microfibril deficient mice. Invest. Ophthalmol. Vis. Sci. 2014;55(13):138.
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© ARVO (1962-2015); The Authors (2016-present)
Recently we found that mice with microfibril deficiencies due to mutations in the fibrillin-1 gene (fbn1) have thin central cornea thickness (CCT). We also found that although microfibril deficient mice have impaired aqueous humor (AH) outflow facility, their intraocular pressure (IOP) is not elevated. Here we test the hypothesis that thin CCT results in underestimation of IOP measured by TonoLab rebound tonometer.
Mice heterozygous for the tight skin mutation of Fbn1 (Tsk+/-) and wild type (WT) controls were used for this study. CCT was determined by spectral domain optical coherence tomography (SD-OCT, Bioptigen). Mice were sacrificed before experiments by carbon dioxide inhalation and eyelid removed. To control IOP, eyes were cannulated with a 33 gauge needle attached to a pressure transducer (Honeywell, 142PC01G) and variable-height fluid reservoir via thick-walled pressure tubing and three-way valve. At various IOPs determined by the fluid column and measured by the pressure transducer (10, 15, 20, 25, 30, 35, 40 and 45 mmHg), TonoLab readings were recorded, each consisting of 6 separate tonometer readings. Calibration curves were generated by plotting TonoLab IOP determination vs. transducer reading. Student T-test was used for statistical analysis.
Tsk+/- mice showed significantly thinner CCT compared with WT mice (70 µm vs. 90 µm, respectively; p=0.008). IOP in Tsk+/- mice was not statistically different from WT mice. Calibration curves showed a linear relationship between TonoLab reading and transducer-determined pressure, with a slope of 1. The calibration curves were nearly identical for Tsk+/- and WT mice.
IOP is not underestimated in Tsk+/- mice despite their much thinner corneas as compared to WT. Lack of elevated IOP in these mice that have decreased outflow facility could be due to compensatory effects such as decreased rate of AH production. Future studies will investigate AH turnover in these mice to explain lack of elevated IOP and investigate differences in ocular compliance associated with thin cornea that may contribute to development of glaucoma without elevated IOP.
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