A LINK BETWEEN TEAR INSTABILITY AND HYPEROSMOLARITY IN DRY EYE.
Liu H, Begley CG, Chen M, Bradley A, Bonanno JA, McNamara N, Nelson JD, Simpson T.
School of Optometry, Indiana University, 800 E atwater ave, Bloomington, Indiana, 47405, United States.
Purpose: Tear film instability and tear hyperosmolarity are considered core mechanisms in the development of dry eye. We hypothesize that evaporation and instability produce transient shifts in tear hyperosmolarity that lead to chronic epithelial stress, inflammation, and symptoms of ocular irritation. The purpose of this study was to (1) provide indirect evidence for short term hyperosmolar conditions during tear instability and to (2) test whether the corneal epithelium responds to transient hyperosmolar stress.
Methods. Five subjects kept one eye open as long as possible and overall discomfort and sensations associated with tear break-up were scaled. Later, the same subjects used the same scales to report discomfort sensations after instillation of NaCl and sucrose hyperosmolar drops (300mOsm/Kg to 1000mOsm/Kg). A two-alternative forced choice experiment was used to obtain osmolarity thresholds. Exp#2: Primary cultured bovine corneal epithelial cells were transiently stressed with the same range of hyperosmolar culture media and pro-inflammatory Mitogen Activated Protein Kinase (MAPKs were measured by western blot).
Results. Tear instability lead to an average discomfort rating of 6.13 and sensations of burning and stinging. These sensations also occurred with hyperosmolar solutions (thresholds between 450-460mOsm/Kg) that required 800-900mOsm/Kg to generate the same discomfort levels reported during tear break-up. MAPK was activated at 600mOsm/Kg of transient hyperosmolar stress.
Conclusion. These experiments provide a link between hyperosmolarity and tear instability, suggesting that hyperosmolar levels in the tear film may transiently spike during tear instability, resulting in corneal inflammation and triggering sensory neurons.
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