Corneal vascularization induced experimentally with corneal extracts.

Corneal oedema with its associated stromal lamellar or fibrillar separation has been proposed as the essential stimulus for corneal vascularization in disease (Cogan, I949). This widely accepted theory was elaborated by Ashton and Cook (I953), who considered that, in addition, a chemical stimulus for vascularization was afforded by a state of "suboxidation" constantly present in corneal tissue. The literature concerning the stimulus for corneal invasion by vessels has been reviewed thoroughly by Ashton (I960). An alternative theory, proposing the release by diseased corneal tissue of a chemical influence for vascular invasion or "vessel-stimulating factor", has been postulated (Campbell and Michaelson, 1949; Maurice, Zauberman, and Michaelson, 1966), but direct evidence of the existence of this factor has not so far been obtained. The relevant arguments for and against it have been fully discussed by Ashton (I 960) and Maurice and others (I966). The latter produced suggestive evidence by implanting fine tubes into the corneal stroma radially disposed to a thermal lesion near the corneal centre. Vessels grew from the corneal periphery into five out of nine tubes open at both ends, but failed to do so in nine tubes of which the central ends were sealed. Diffusion of a chemical substance from the lesion was invoked to explain these findings. If a chemical stimulus for invasion of the cornea by vessels is released in pathological states by damaged or diseased corneal tissue, it might be possible experimentally to injure the cornea in a way that would be expected to lead to vascularization, and then to excise, homogenize, and extract that cornea, and to induce vascularization by applying the extract by a suitable means to a normal cornea. This principle was investigated in the adult Dutch rabbit in the following experiments.