ON THE ACTION OF PROSTAGLANDIN E1 AND PROSTAGLANDINS FROM BRAIN ON THE ISOLATED RAT STOMACH

1966 ◽  
Vol 44 (6) ◽  
pp. 933-950 ◽  
Author(s):  
F. Coceani ◽  
L. S. Wolfe
Keyword(s):  
Calcium Influx ◽  
Direct Action ◽  
Metabolic Inhibitors ◽  
Prostaglandin E ◽  
Metabolic Reaction ◽  
Rat Stomach ◽  
Unsaturated Carboxylic Acids ◽  
External Potassium ◽  
Stomach Fundus ◽  
Isolated Rat

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.

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
Keyword(s):  
Brain Tissue ◽  
Alkali Treatment ◽  
Water Soluble ◽  
Rat Stomach ◽  
Tissue Extracts ◽  
Slow Type ◽  
Stomach Fundus ◽  
Acid And Alkali Treatment ◽  
Layer Chromatography ◽  
Isolated Rat

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.

CSF smooth-muscle constrictor activity associated with cerebral vasospasm and mortality in SAH patients

1984 ◽  
Vol 60 (5) ◽  
pp. 927-934 ◽  
Author(s):  
Andrew H. Kaye ◽  
Philip C. Tagari ◽  
Peter J. Teddy ◽  
Christopher B. T. Adams ◽  
William P. Blaso ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intracranial Aneurysms ◽  
Prostaglandin E ◽  
Rat Stomach ◽  
Content Type ◽  
Group Of Seven ◽  
Angiographic Vasospasm ◽  
Stomach Fundus ◽  
Subarachnoid Blood ◽  
Ruptured Intracranial Aneurysms

✓ Cerebrospinal fluid (CSF) was collected preoperatively (by lumbar puncture) or perioperatively (by lumbar or ventricular drain) from 32 patients with subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms. Samples were also obtained from six control patients without evidence of subarachnoid blood. Smooth-muscle constrictor activity in the CSF was measured by bioassay using the isolated rat stomach fundus preparation. Concentrations of unidentified smooth-muscle constrictor substances were considerably greater in CSF from a group of seven patients with evidence of severe angiographic vasospasm and/or delayed ischemic deficits who died (73.8 ± 39.7 nmol/liter prostaglandin E2 (PGE2) equivalents), as compared to 25 other SAH patients who survived (6.5 ± 1.4 nmol/liter PGE2 equivalents), and six control patients (1.17 ± 0.34 nmol/liter PGE2 equivalents). The data suggest that there is a relationship between smooth-muscle constrictor substances in the CSF after SAH and both the degree of angiographic vasospasm and the outcome. It is possible that this relationship might be exploited clinically.

Catabolism of 6-keto prostaglandin E1 by rat kidney homogenates

1984 ◽  
Vol 62 (8) ◽  
pp. 709-714 ◽  
Author(s):  
C. R. Pace-Asciak ◽  
S. Micallef
Keyword(s):  
Mass Spectrometry ◽  
Chemical Ionization ◽  
Rat Kidney ◽  
Trimethylsilyl Ether ◽  
Negative Ion ◽  
Electron Capture Detection ◽  
Prostaglandin E ◽  
Rat Stomach ◽  
Negative Ion Chemical Ionization ◽  
Stomach Fundus

6-Keto prostaglandin E1 (PGE1) was catabolized into two major products by homogenates of rat kidney in the presence of NAD. Rat brain was mostly deficient in this catabolic activity. A total profile of products from these experiments could be obtained using the pentafluorobenzyl esters, O-methyloxime, and trimethylsilyl ether derivatives and analysis by capillary gas chromatography with electron capture detection. The same samples could be effectively analyzed by mass spectrometry using negative ion chemical ionization (NICI) detection. While 6-keto PGE1 showed spasmogenic activity on the rat stomach fundus as well as inhibition of the ADP-induced platelet aggregation, its catabolites lacked such activity. Analysis of rat whole blood by mass spectrometry using the NICI technique showed the presence of small amounts of 6-keto PGE1 and its 15-keto and 15-keto 13, 14-dihydro catabolites in two of eight blood samples.

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