With 3 Figures
It is a well known fact that the cornea has a great swelling capacity so that it will swell considerably even when placed in blood serum, and that the cornea in vivo is kept dehydrated to some extent. The mechanism for this dehydration, however, is still not very well known. The epithelial and endothelial layers can act as semipermeable membranes, so that solutions of various concentrations in contact with the surface can make the cornea thinner if they are hypertonic and thicker if they are hypotonic as shown by COGAN β’ KINSEY (1942) on excised eyes and by VON BAHR (1948, 1956 a, b) on living eyes. As the tears as well as the aqueous humour are hypertonic to blood plasma the theory has been developed that the deturgescence of the cornea is caused by osmotic forces. This theory has met severe criticism and experiments with radioactive isotopes (POTTS et al., 1950) on living eyes and studies on the metabolism of the cornea in various conditions (LANGHAM, 1954; SCHWARTZ, DANES tfr LEINFELDER, 1954;DAVSON 1955; HARRIS & NORD-QUIST, 1955) have given good reasons for the assumption of some vital activity of the cellular constituents of the cornea for the dehydration of the cornea.
In measurements of the thickness of the human cornea in the evening and just after the opening of the eyes in the morning I have found no difference. As there is no evaporation from the tear film during sleep the tear fluid should be isosmotic with the tissues and should not have any osmotic effect on the cornea during sleep. The thickness of the cornea does not increase, however, and this shows that osmotic action through the epithelial surface cannot be essential for the corneal deturgescence.
Similar measurements have now been performed when the anterior chamber was perfused with an artificial aqueous humour the tonicity of which was varied by variations in the concentration of sodium chloride.