advertisement
A sensor on the contact lens for continuous IOP monitoring has advanced in glaucoma diagnostics. This report, taking another step forward, demonstrates that a platform using contact lens and nano-engineering innovations to integrate diagnostics and therapeutics of an elevated IOP is achievable. The authors showed that the release of timolol, a beta-blocker, from the reservoir on the contact lens could be triggered by the IOP sensor also on the contact lens and consequently reduced IOP in New Zealand albino rabbits. Such an on-demand delivery of IOP lowering medication is desirable for practicing personalized glaucoma treatment in the future. However, morphological results on the retina presented in the report do not go along with our current understanding of using rabbits as a glaucoma model. Despite a few well-established experimental methods to raise IOP in this animal species, high IOPs generally do not lead to glaucomatous changes in the inner layer of retina. The difficulty in rabbits may be due to poorly developed lamina cribrosa-like structures as well as myelinated axons of retinal ganglion cells near the optic nerve head. In addition, the role of ocular beta-adrenergic activity in the regulation of rabbit IOP is insignificant; a 'normal' timolol dose for the rabbit eye may only cause a small IOP reduction. An eyedrop of 0.5% timolol used by glaucoma patients is probably a supramaximal dose for systemic absorption by a two-kg rabbit. This supramaximal timolol dose can significantly alter the cardiovascular parameters and indirectly change IOPs in the paired eyes. On the other hand, local bioavailability of timolol after an eyedrop administration in albino rabbits is short in time due to the lack of ocular pigments as a natural depot. Needless to say, more research is warranted to clarify the exact mechanisms responsible for the interesting morphological observations in this report.