Review: Mediation of the Ocular Response to Injury

Abstract

The structures of the anterior segment of the eye provide aqueous humour for metabolic traffic, regulation of intraocular pressure and the maintenance of a functional permeability barrier to separate internal compartments from general systemic influences. Irritative and injurous insults to the eye elicit an acute defensive miotic and vascular response which upsets the aqueous dynamics and provokes the influx of blood plasma proteins into the aqueous chambers. These events are initiated by antidromic activation of sensory elements within the anterior segment, releasing substance P and calcitonin gene-related peptide (CGRP) which, in lower mammals at least, stimulate respectively the miotic and vascular reactions. Considerable species differences can be found in the responsiveness of the eye to injury and in the effects of exogenous CGRP and substance P. OCULAR INJURY RESPONSE

Evaluation of short-term increased intraocular pressure on flash- and pattern-generated electroretinograms of dogs

“…All dogs received flunixin meglumine f (0.11 mg/kg, IV) after induction of anesthesia to prevent fibrin formation and miosis caused by inflammation that develops secondary to intraocular cannulation. 11 Mydriasis, using mydriatic drops, g was achieved prior to general anesthesia. A 22-or 20-gauge arterial catheter (filled with heparin) was inserted into the dorsal pedal artery of each dog on day 0.…”

Role of nitric oxide (NO) in ocular inflammation

“…There is much evidence to suggest that C-fibre neurotransmitters, such as substance P and calcitonin gene-related peptide (CGRP), play a key role in the ocular response to injury (Stone et al, 1987;Unger, 1990). As there is no barrier separating the iris and the ciliary body from the anterior chamber, any agent that is released locally will diffuse into the anterior chamber, making the eye an excellent model for studies of transmitter release.…”

Tear production and intraocular pressure in canine eyes with corneal ulceration

“…The functional unit regulates the major components of the tear film in order to protect the ocular surface. Painful stimulation of the eye is known to result in tear secretion and other reflexes to prevent the eye from potential damage (Unger, 1990;Belmonte et al, 1997;Situ and Simpson, 2010) but there is little in the literature to show a direct link of increased tear secretion with corneal ulceration. The IOP occurs through a balance between the production of aqueous humour and its drainage through the iridiocorneal angle (conventional outflow) and through the uveoscleral pathways (unconventional outflow) (Reinstein et al, 2009).…”

“…Burg Open Veterinary Journal, (2017), Vol. 7(2): 117-125 ________________________________________________________________________________________________________ It has been previously documented that after an initial rise in IOP following ocular surface injury, a prolonged reduction in IOP is usually found (Unger, 1990). An antidromal trigeminal reflex arc is considered to be responsible for this hypotony, predominantly caused by a prostaglandin induced increase in unconventional aqueous outflow (Camras et al, 1977;Fine et al, 2007).…”

“…One previous paper has documented that the STT in dogs with corneal epithelial defects is significantly greater when compared to the contralateral unaffected eyes ), a result confirmed in this study, but in that report the change in tear production was but a marginal note in a larger study of superficial epithelial erosions: here we extend the investigation to a greater number of ulcerated eyes with ulcers of different types and depths. The most likely cause of increased tear production in corneal ulceration is the interaction of corneal nociceptive stimulation and subsequent lacrimal secretion (Unger, 1990). The cornea is one of the most richly innervated tissues in the body receiving dense innervation by sensory nerves predominantly originating from neurons located in the ipsilateral trigeminal ganglion and modest sympathetic innervation from the superior cervical ganglion.…”