Release of Prostaglandins in Ocular Inflammation in the Rabbit

Summary1. The bovine isolated sphincter pupillae incubated in Krebs solution releases a biologically active substance tentatively identified as prostaglandin E2. 2. The prostaglandin did not appear to be of neural origin or to result merely from tissue degeneration.3. The spontaneous release of prostaglandin E,-like material was related to the tone of the sphincter. Output increased as tone was acquired after setting up the tissue and fell when various procedures were used to reduce the tone. 4. Low concentrations of E and F-type prostaglandins produced slow, wellsustained contractions of the atonic sphincter, prostaglandin E2 being the most potent of those tested. The responses to prostaglandin EB were antagonized selectively by a prostaglandin antagonist SC-19220 (a dibenzoxazepine derivative) which in higher concentrations caused dose-dependent relaxations of the preparation. 5. Prostaglandins did not appear to modulate transmission from nerve to muscle in the sphincter. 6. The hypothesis that prostaglandin E2 might be produced to act as a local hormone causing tonic contraction of the sphincter pupillae is discussed.

Section: Introductionmentioning

confidence: 99%

Prostaglandin E₂ and the bovine sphincter pupillae

Posner

1973

“…Increased amounts ofE prostaglandin are found in inflamed skin (Sondergaard & Greaves, 1970;Greaves, Sondergaard & McDonald-Gibson, 1971; Angaard & Jonsson, 1971;Hamberg & Jonsson, 1973), in ocular (Eakins, Whitelocke, Perkins, Bennet & Ungar, 1972) and in many other types of inflammation (Ferreira, Flower, Moncada & Vane, 1975).…”

Section: Introductionmentioning

confidence: 99%

INFLAMMATORY EFFECTS OF PROSTAGLANDIN D₂ IN RAT AND HUMAN SKIN

Flower

Harvey

Kingston

1976

187

I Intradermal injection of prostaglandin (PG) D1 and D2 in the human forearm produced a longlasting dose-related erythema. When compared with prostaglandin E1 or E2 the order of potency for erythema production was PGE1 > PGE2 > PGD2 > PGD1. 2 In rat skin, prostaglandin D2 but not D1 caused an increase in vascular permeability as quantitated by the Evans blue method and the 251I-albumin extravasation technique. Prostaglandin E2 was 3-5 times more potent than prostaglandin D2. 3 Prostaglandin D2 (10 ng) potentiated the increase in vascular permeability in rat skin produced by histamine, but not that produced by bradykinin. 4 Prostaglandin D2 (10, 20 and 50 ng) did not elicit oedema or hyperalgesia in the rat paw oedema test, but potentiated carrageenan-induced oedema; hyperalgesia was potentiated by doses of 100 ng and above.

“…Eakins, Whitelocke, Perkins, Bennett & Unger (1972) and Eakins, Whitelocke, Bennett & Martenet (1973) demonstrated the release of prostaglandins into the aqueous humour of rabbits and man with acute ocular inflammation.…”

Section: Introductionmentioning

confidence: 99%

Release of Prostaglandin‐like Substances by Shigella Endotoxin and Its Inhibition by Non‐steroidal Anti‐inflammatory Compounds

Bhattacherjee

1975

1 The effects of intravenous and intraocular injections of Shigella endotoxin on the inflammatory response, the release of prostaglandin-like substances into the aqueous humour, and the effects of indomethacin on the inflammatory response were studied in the rabbit eye. 2 Both intravenous and intraocular injection of endotoxin released 12.8 ng to 72 ng of prostaglandin-like substances per ml of aqueous humour and increased the permeability of the blood-aqueous barrier as shown by the rise in aqueous humour protein (26-52 mg protein/ml of aqueous humour). 3 Indomethacin, 0.25% administered topically completely inhibited the release of prostaglandin-like substances but was found to have inconsistent inhibitory effects on the clinical signs of inflammation and on the blood-aqueous barrier. Indomethacin was less effective in eyes receiving the higher dose of endotoxin. 4 It is suggested that prostaglandins and possibly other chemical mediators are involved in endotoxin-induced ocular inflammation.