The possible roles of prostaglandins and a neural pathway in the disruption of the blood-aqueous barrier in the rabbit eye after cyclocryocoagulation were studied. Both the preoperative IV administration of the prostaglandin inhibitor acetylsalicylic acid and the application of retrobulbar and topical anesthesia reduced IOP and decreased breakdown of the blood-aqueous barrier, as measured by protein in the aqueous humour. These results imply that the acute response of the animal eye to cyclocryocoagulation is mediated partly by prostaglandins and partly by a neural component resistent an inhibitor of prostaglandin synthesis. When administered together, acetylsalicylic acid and ocular anesthesia yielded a further reduction in postoperative reactions and protein concentrations in the aqueous humour, but were unable to abolish the ocular response completely. The dual ocular mediation to cyclocryocoagulation is apparently due to the combined thermal and mechanical injury caused to ocular structures which synthesize prostaglandins and receive sensory innervation from the trigeminal nerve. The considerable breakdown of the blood-aqueous barrier in cyclocryocoagulation allows leakage of different molecular weight proteins, in equal ratio, into the aqueous humour.

R. Haddad

G. Grabner

G. Strasser

Mediation of the ocular response to cyclocryocoagulation

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