Effect of mechanical stimulation on rabbits' eyes: release of active substance in anterior chamber perfusates

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

“…The use of the sensitive colon preparations from Meriones libycus for irin, and later prostaglandin, assays was introduced by Ambache et al (1965). The species is now known as Meriones shawi (Ambache et al, 1966;Ambache & Brummer, 1968).…”

Section: Jird Colonmentioning

confidence: 99%

Antagonism of some smooth muscle actions of prostaglandins by polyphloretin phosphate

Eakins

Karim

Miller

1970

Summary1. The antagonism of the smooth muscle stimulating actions of PGF2a and PGE2 by polyphloretin phosphate (PPP) was studied on several isolated smooth muscle preparations and on the blood pressure of the anaesthetized rabbit. 2. PPP (2'5-20 ,ug/ml) reversibly inhibited contractions of the jird colon produced by PGE2 or PGF2a; PGF2a was more readily antagonized than PGE2. 3. PPP (2S5-30 jug/ml) reversibly antagonized contractions produced by PGE2 and PGF2a on the isolated rabbit jejunum and uterus. In these preparations PPP antagonized PGE2 as readily as PGF2a. 4. It is concluded that PPP is a selective antagonist to the prostaglandins on these tissues, for contractions produced by other agonists, such as acetylcholine, angiotensin, 5-hydroxytryptamine and bradykinin were not reduced by concentrations of PPP which markedly antagonized responses to the prostaglandins. 5. Intravenous injections of PPP (25-200 mg/ kg) resulted in a variable antagonism to the fall in blood pressure produced by intravenous injections of PGF2a in the anaesthetized rabbit; vasodepressor responses produced by PGE2 and acetylcholine were not antagonized. 6. The mechanism of this antagonism by PPP is not clear and must await further investigation.

“…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)