PROSTAGLANDINS IN BRAIN AND THE RELEASE OF PROSTAGLANDIN-LIKE COMPOUNDS FROM THE CAT CEREBELLAR CORTEX

1965 ◽  
Vol 43 (3) ◽  
pp. 445-450 ◽  
Author(s):  
F. Coceani ◽  
L. S. Wolfe

A water-soluble lipid material resistant to acid and alkali treatment was found in perfusates and extracts of brain tissue, which induced contraction of the 'slow type' on the isolated rat stomach fundus. The material isolated from brain tissue extracts behaved in solvent partition systems like the prostaglandin compounds and could be purified by silicic acid and thin-layer chromatography. The smooth-muscle-stimulating activity is likely due to the trihydroxyprostaglandin compounds.

1968 ◽  
Vol 57 (3) ◽  
pp. 395-404 ◽  
Author(s):  
K. H. Raisinghani ◽  
R. I. Dorfman ◽  
E. Forchielli ◽  
L. Gyermek ◽  
G. Genther

ABSTRACT A method has been developed for the detection, isolation and quantitation of progesterone, pregnanolone and pregnanedione in brain tissue of rats receiving pharmacological hypnotic doses of these three substances. Prior to extraction radioactive tracers were added to brain tissue obtained from animals receiving these agents and the brain tissue extracts were purified by paper and thin layer chromatography. The material administered as well as some of the major metabolites were quantitated by gas liquid chromatography, and corrections for losses throughout the entire procedure and up to injection into GLC were based on recovery of added radioactive markers. The possible significance of the conversion of progesterone into hypnotically more potent metabolites is discussed.


1966 ◽  
Vol 44 (6) ◽  
pp. 933-950 ◽  
Author(s):  
F. Coceani ◽  
L. S. Wolfe

Prostaglandins are a group of structurally related dihydroxyketo- and trihydroxy-C20 unsaturated carboxylic acids which cause contraction of intestinal smooth muscle at concentrations down to 1 × 10−10 g/ml. Crystalline prostaglandin E1 and a purified preparation of ox brain prostaglandins (mainly F2α) initiated contraction of the isolated rat stomach fundus preparation by a direct action on the muscle which was strongly antagonized by adrenalin and noradrenalin. Drugs that inhibited sympathetic fibers or receptors potentiated the action of prostaglandins, whereas drugs that stimulated sympathetic receptors were inhibitory. Prostaglandin action was greatly diminished by lowering the temperature from 37 °C to 24 °C. The presence of oxygen was absolutely necessary for initiation of prostaglandin contraction but not for acetylcholine contraction. Prostaglandins were taken up by the tissue or produced a persistent change when added under anoxic conditions, but were unable to act unless oxygen was present. Metabolic inhibitors such as cyanide, azide, and carbon monoxide reversibly inhibited prostaglandin action to a greater extent than that of acetylcholine. A tonic rebound contraction occurred after removal of these inhibitors. Ascorbic acid and reduced (but not oxidized) glutathione reversibly enhanced prostaglandin action. Increased external potassium progressively increased the sensitivity of the muscle to prostaglandins. A hypothesis is proposed in which prostaglandins in association with an oxygen-requiring metabolic reaction initiate contraction by the release of bound calcium or the facilitation of calcium influx.


Pharmacology ◽  
1977 ◽  
Vol 15 (2) ◽  
pp. 118-126 ◽  
Author(s):  
Z.S. Ercan ◽  
R.K. Türker

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