Prostaglandin-mediated contractile effect of impromidine and dimaprit in the isolated rat stomach fundus

1981 ◽  
Vol 37 (10) ◽  
pp. 1092-1093
Author(s):  
Z. S. Ercan
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.


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

2001 ◽  
Vol 120 (5) ◽  
pp. A159-A159
Author(s):  
S RO ◽  
K YAKABI ◽  
T NAKAMURA

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