Influence of the Fifth Cranial Nerve on the Intra-Ocular Pressure of the Rabbit Eye

116

Six to eight days after diathermic destruction of the fifth cranial nerve in the rabbit, the ocular hypertensive and miotic responses to intracameral administration of capsaicin, bradykinin, and prostaglandin E1 were greatly reduced or completely abolished. The response to substance P was not abolished. A response could still be obtained to chemical irritants 36 h after coagulation of the nerve and it is deduced that manifestation of the response is dependent upon functional sensory nerve terminals, and is independent of central connections. It is suggested that prostaglandin E1 and bradykinin act directly upon the sensory nerve endings and that propagation of the response is augmented by axon reflex. In view of the ability of substance P to induce miosis in the denervated eyes, it is presumed that its actions are not mediated via sensory nerves. It is considered possible that the mediator(s) released from sensory nerve endings after chemical irritation or antidromic stimulation may act in the same way as substance P with regard to the miotic effect. Synthetic substance P will only produce ocular hypertension in doses which induce a maximal miotic response. This may either be a question of access or a partial resemblance to the endogenous mediator.

Section: Discussionmentioning

confidence: 99%

THE EFFECTS OF SENSORY DENERVATION ON THE RESPONSES OF THE RABBIT EYE TO PROSTAGLANDIN E₁, BRADYKININ AND SUBSTANCE P

Butler

Hammond

1980

116

“…Thus, there was good evidence that prostaglandins are involved in the response of the rabbit eye to irritation. It was also well known that the raibbit eye responds to chemical or mechanical irritation with a prolonged miosis, vasodilatation, increased capillary permeability and a sustained rise in IOP (Duke-Elder & Duke-Elder, 1931 ;Davson & Quilliam, 1947 ;Perkins, 1957); these effects cannot be prevented by the previous administration of atropine and mepyramine (Ambache et al, 1965), and the prolonged miosis is mimicked both in vivo and in vitro by the administration of irin (Ambache, 1956(Ambache, , 1957. This strongly suggests that both vascular effects and alterations in the permeability of the blood-aqueous barrier are in,fact involved in the IOP response of rabbits to prostaglandins.…”

Section: Intracameral Injections Of Prostaglandins E1 and E2 Resultedmentioning

confidence: 99%

The effects of prostaglandins on the intraocular pressure of the rabbit

Beitch

Eakins

1969

208

1. The effects of intracameral injections of prostaglandins E1, E2, Fia, F2a, and A1 were studied on.the intraocular pressure (IOP) of rabbits anaesthetized with urethane.2. With the exception of prostaglandin F,a, all the prostaglandins studied were found to be capable of producing a large, sustained rise in IOP, accompanied in many cases by miosis. 3. A marked decrease in response to repeated injections was found with all the prostaglandins studied; this effect was more pronounced following a large initial response to the prostaglandin. 4. The descending order of potency in their ability to raise IOP was as follows: prostaglandin Ei-E2>F2a>Al>Fia.5. Intracameral injections of prostaglandins E1 and E2 resulted in an increase in the protein content of the aqueous humour, which was related to the magnitude of the sustained increase in IOP. 6. Stabilization of the blood-aqueous barrier with polyphloretin phosgphate markedly reduced both the IOP response and the effect of prostaglandin E2 on the protein content of the aqueous humour. 7. It is concluded that the production of local vasodilatation and increased permeability of the blood-aqueous barrier play an important part in the effect of prostaglandins on the IOP. The involvement of prostaglandins in the response of the rabbit eye to irritation is discussed.Injections of prostaglandins into rabbit eyes have been shown by Waitzman & King (1967) to produce a sustained rise in intraocular pressure (IOP). This effect on the IOP was thought to result from an action of prostaglandins on the metabolic processes involved in aqueous humour production, rather than from vascular or permeaibility changes (Waitzman, 1968), although it was well known that many prostaglandins are powerful vasodilators. Moreover, it had been shown earlier that the response of the rabbit eye to irritation is associated with the release into the aqueous humour of irin, an ether-soluble spasmogen with vasodilator activity consisting of unsaturated hydroxy fatty acid(s)

“…In the eye, neurogenic inflammation occurs in response to traumatic stimuli, such as laser therapy of the eye and ocular surgery (Caprioli et al, 1985) and it consists of vasodilatation in the anterior uvea, breakdown of the blood-aqueous barrier, increase in the intraocular pressure (IOP) and miosis (Perkins, 1957).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of methysergide on calcitonin gene‐related peptide‐induced vasodilatation and ocular irritative changes in the rabbit

Krootila

Oksala²,

Zschauer

et al. 1992

1 Calcitonin gene-related peptide (CGRP) is involved in ocular neurogenic inflammation in the rabbit, causing vasodilatation in the anterior uvea, breakdown of the blood-aqueous barrier, increase in the intraocular pressure (IOP) and rise in the adenosine 3':5'-cyclic monophosphate (cyclic AMP) content in the aqueous humour. So far there is no means of preventing these CGRP-induced ocular effects. 2 In the present study, the effect of intravenous methysergide (1-10 mg kg-', b.w.) on CGRP-induced changes in the IOP, blood-aqueous barrier and cyclic AMP content in the aqueous humour was studied in vivo. The effect of methysergide on CGRP-induced vasodilatation both in vivo and in vitro was also investigated. 3 Methysergide decreased intraocular pressure but had only a transient effect on blood pressure. Methysergide decreased the regional blood flow in ocular tissues by 53-65%, but did not have such a vasoconstrictor effect in most extra-ocular tissues studied. 4 Methysergide inhibited CGRP-induced vasodilatation, increase in the TOP, breakdown of the bloodaqueous barrier and increase in the cyclic AMP content in the aqueous humour in vivo. 5In vitro, methysergide alone did not have effects on the vascular tone in isolated ophthalmic artery of rabbit. However, it potentiated noradrenaline (NA)-induced contraction. There were no differences in the IC50 values for CGRP on the NA-induced contraction in the presence and absence of methysergide, indicating that methysergide has no direct effect on the vasorelaxant effect of CGRP in vitro. 6 The present study demonstrates that in the rabbit eye methysergide inhibits CGRP-induced changes. One inhibitory mechanism of methysergide may be to enhance the effect of a vasoconstrictor (NA) to antagonize the vasodilator effect of CGRP. The present findings suggest that a methysergide-sensitive mechanism may be used to limit some pathophysiological conditions in the eye that involve neurogenic inflammation and the release of CGRP.