Metabolism of prostaglandin endoperoxide in animal tissues

Sun, Frank F.; Chapman, Justin; McGuire, James C.

doi:10.1016/0090-6980(77)90285-4

Cited by 279 publications

(48 citation statements)

References 18 publications

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“…6-Keto-PGF-la has been identified in several organs and tissues (Sun, Chapman & McGuire, 1977). We found very low concentrations in the semen and the presence of prostacyclin in this fluid is therefore probably unimportant.…”

Section: Human Semenmentioning

confidence: 49%

Radioimmunoassay of prostaglandins in the semen of fertile men

Gerozissis¹,

Dray²

1981

Reproduction

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Section: Human Semenmentioning

confidence: 49%

Radioimmunoassay of prostaglandins in the semen of fertile men

Gerozissis¹,

Dray²

1981

Reproduction

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“…The dose-response differences in endotoxin on thromboxane and prostacyclin production could reflect a role for endotoxin in modifying pathways within the arachidonic acid cascade. More likely, however, is the alternative explanation that prostacyclin synthetase is very active but easily saturated (34). Thus, at low doses of endotoxin with only small amounts of arachidonic acid being converted to the intermediary cyclic endoperoxides, prostacyclin synthetase is at least equal to thromboxane synthetase but at higher doses of endotoxin with more arachidonic acid entering the cascade, prostacyclin synthetase is saturated allowing more cyclic endoperoxides to be diverted to thromboxane or other prostanoids.…”

Section: Resultsmentioning

confidence: 99%

Role of Thromboxane and Prostacyclin in Pulmonary Vasomotor Changes after Endotoxin in Dogs

Hales¹,

Sonne²,

Peterson³

et al. 1981

J. Clin. Invest.

139

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A B S T R A C T Cyclooxygenase inhibitors prevent the pulmonary vasomotor changes in response to low-dose endotoxin. We, therefore, explored the role of two highly vasoactive prostanoids, thromboxane A2, a vasoconstrictor, and prostacyclin, a vasodilator, in the transient pulmonary vasoconstriction and subsequent loss of alveolar hypoxis vasoconstriction (AHPV) that follows endotoxin. AHPV was tested in the dog with a double-lumened endotracheal tube allowing ventilation of one lung with nitrogen as a hypoxic challenge while the other lung was ventilated with oxygen to maintain systemic oxygenation. Relative distribution of perfusion to the two lungs was assessed with intravenous 133Xe and external scintillation detectors. The stable metabolites of thromboxane and prostacyclin, i.e., thromboxane B2 and 6-keto-prostaglandin F1,a were measured in plasma with radioimmunoassay. 15 ,ug/kg i.v. ofendotoxin induced no rise in pulmonary vascular resistance (PVR), but prevented AHPV so that the initial 33% (±2 SEM) decrease in perfusion to the hypoxic lung became only a 2% (± 1) decrease. Circulating levels of thromboxane and prostacyclin concurrently rose (P < 0.01) from nondetectable levels to 380 pg/ml (±40) and 360 pg/ml (±130). 150 ,g/kg of endotoxin induced a transient rise in PVR from 4.09 to 9.00 mm Hg/liter per min in association (r = 0.89, P < 0.01) with a sharp rise in thromboxane levels to 4,460 pg/ml (± 1,350) whereas prostacyclin levels were elevated less markedly to 550 pg/ml (+400). Prostaglandin F2<,X another vasoconstrictor, was not elevated. 30 min after endotoxin when PVR was again base line and AHPV lost, thromboxane fell significantly (P < 0.01) to 2,200 pg/ml (± 1,100) whereas prostacyclin remained elevated at 360 pg/ml (±135), a level similar to that seen when 15 ,g/kg of endotoxin induced Dr. Peterson is an Established Investigator ofthe American Heart Association.

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“…The residue was subjected to thin-layer chromatography (TLC) to separate PGE2-TX and 6-keto-PGFI« with Analtech 0.25 mm silica gel G precoated plates. An organic phase consisting of ethylacetate : acetic acid: isooctan : H2O (110:20:50:100) was used for developing (Sun et al 1977). PGE2, 6-keto-PGFI« and TXB2 were determined by radioimmunoassay using 3H-PGE2, 3H-6-ketoPGFI«, 3H-TXB2 (New England Nuclear) and antisera.…”

Section: Determination O F Gastric Mucosal Lesionsmentioning

confidence: 99%

Effect of gefarnate on endogenous prostacyclin, prostaglandin E2 and thromboxane in water-immersed rats.

Kobayashi

Nakamura

Chono

et al. 1983

Tohoku J. Exp. Med.

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The level of endogenous prostacyclin (PGI2), prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) in rat gastric mucosa was determined by radioimmunoassay to examine whether gefarnate, an antiulcer agent, maintained the endogenous prostaglandin (PG) level in rats subjected to waterimmersion stress. Seven-hr immersion induced gastric lesions and a marked reduction in PGI2 and PGE2. When gefarnate was injected subcutaneously before stress exposure, the mean ulcer index was reduced and the PGI2 and PGE2 levels were maintained. Our results suggest that the reduction of endogenous PGI2 and PGE2 is a major factor in water-immersion-induced ulcers in rats, and that gefarnate inhibits this ulcer formation by inhibiting a reduction in those PGs induced by water-immersion stress prostacyclin (PGI2); prostaglandin E2 (PGE2); thromboxane A2 (TXA2); gefarnate; gastric mucosa

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Metabolism of prostaglandin endoperoxide in animal tissues

Cited by 279 publications

References 18 publications

Radioimmunoassay of prostaglandins in the semen of fertile men

Radioimmunoassay of prostaglandins in the semen of fertile men

Role of Thromboxane and Prostacyclin in Pulmonary Vasomotor Changes after Endotoxin in Dogs

Effect of gefarnate on endogenous prostacyclin, prostaglandin E2 and thromboxane in water-immersed rats.

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