Recently, the Meniere’s research laboratory has been exploring the development of a novel treatment for endolymphatic hydrops. The premise is that if a chemical could be applied to the inner ear which temporarily increased the permeability of the endolymphatic compartment, it may provide hydrostatic relief of hydrops (kind of like deflating a balloon for a while). Currently, there are a host of chemicals that are used in pharmacology, and are FDA and TGA approved, which provide such a temporary (i.e. hours) increase in the permeability of membranes.
We began trialing ‘sodium caprate’, which is often used to temporarily permeabilize the lining of the intestines, but has recently been used to increase the fluid permeability of inner ear tissues. At moderate concentrations, sodium caprate certainly increases the permeability of membranes like the vasculature overlying the cochlea:
Right) The outer vasculature of the cochlea imaged using our Light Sheet Microscope, with fluorescent contrast agents perfused through blood. Left) In an ear where 20mM sodium caprate has been applied to the middle ear, demonstrating the blood vessels are permeabilized and leak blood onto the cochlear wall. Images are presented in low-resolution.
Moreover, sodium caprate can be applied at lower concentrations, directly to the endolymphatic compartment, increasing its permeability, and allowing perilymph and endolymph to mix temporarily. However, we have yet to perfect methods of applying sodium caprate via and intra-tympanic approach (which would be used clinically), enabling endolymph compartment to be temporarily permeabilized. We currently believe this is due to the complex pharmacokinetics of the inner ear, which make drug delivery to the inner ear a tricky business.