Effect of Rapid Depressurization on Cultured Cells

The importance of intraocular pressure in the pathology of damage to the optic nerve in glaucoma is well known. While the precise mechanism by which elevated pressure leads to damage is unknown, it presumably involves elevated tissue strain levels caused by pressure gradients in this tissue. However, in recent years an alternate hypothesis has been forwarded that hydrostatic pressure itself, not gradients, can damage ocular tissues. This has lead to a variety of studies applying hydrostatic pressure to cells and determining the effects on cell function. Such studies are particularly attractive because of the simplicity in their design. A large number of studies have been done using this methodology (see Lei et al. for literature citations {Lei, 2011 #5581}) but questions have been raised as to both the relevance of such studies to glaucoma and whether artifacts in such studies invalidate their conclusions {Ethier, 2006 #4842; Johnson, 2007 #5580; Lei, 2011 #5581}. In particular, Lei et al. showed that elevated hydrostatic pressure achieved by a hydrostatic column causes a decreased oxygen tension available to the tested cells leading to hypoxia. However, a second method of raising hydrostatic pressure used in such studies, namely increasing the pressure of a gas supply in equilibrium with the perfusion fluid delivered to the cells, was not directly examined by Lei et al. (although they did comment how this approach might also be subject to artifact). Since this latter approach is still being used to examine the effects of hydrostatic pressure on cell function (e.g. {Liu, 2012 #5578}), it seems important to determine why this method, which increases rather than decreases the oxygen available to cells, has an effect on cell function (we presume this is not due to the hydrostatic pressure itself, but we remain open-minded). Cell function has been assessed in all of the previous hydrostatic pressure studies after relief of the hydrostatic pressure that the cells a