Sensory mediation of the ocular response to neutral formaldehyde

Topical application of 100 or 250 μg neutral formaldehyde to the rabbit eye elicits an acute inflammatory response consisting of a raised intraocular pressure (IOP), anterior uveal vasodilation, miosis and an increase in protein in the aqueous humour. Prior treatment with 0·4% benoxinate (12 drops over 30 min) inhibited these ocular changes whereas systemic indomethacin or atropine pretreatment had no notable effect. No raised levels of prostaglandin-like activity were observed in any samples of aqueous humour withdrawn 15 min after stimulation with formaldehyde. The major site of breakdown of the blood-aqueous barrier was shown by fluorescein angiography and colloidal carbon vascular “labelling” to occur in the ciliary processes.The IOP response to 6–50 μg formaldehyde administered intracamerally during closed circuit perfusion was greatly reduced by benoxinate or intracamerally infused tetrodotoxin. Furthermore the response was essentially abolished in eyes in which the ipsilateral sensory nerve supply had been destroyed by diathermic coagulation of the ophthalmic branch of the trigeminal nerve. The response to submaximal doses of formaldehyde was greater in the unilaterally sympathectomized eye than in the fellow control eye.These observations indicate that the ocular response to this form of chemical irritation is dependent largely, if not entirely, upon a non-prostaglandinergic and non-cholinergic excitatory pathway most likely occurring in sensory nervous elements.