Showing papers in "Prostaglandins in 1979"

TL;DR: It was suggested that the peripheral analgesic effect of morphine is due to an inhibition of adenylate-cyclase activity.

TL;DR: Cyclic GMP as well as agents which interfere with Ca2+ influx (verapamil and lanthanum) were local analgesics in normal and hyperalgesic paws, and PGE2, dibutyryl cyclic AMP, and methyl-xanthines caused a dose dependenthyperalgesia.

TL;DR: It is proposed that SRS is formed from a previously described unstable epoxide intermediate in the formation of dihydroxylated arachidonic acid metabolites in leukocytes and introduced for compounds which like SRS are non-cyclized C20 carboxylic acids with one or two oxygen substituents and three conjugated double bonds.

TL;DR: The ability of partially purified human and guinea-pig haematogenous cell populations, when cultured in vitro, to metabolise arachidonic acid (AA) has been studied and the proposed role of prostaglandins as mediators and modulators in immunopathology is discussed.

TL;DR: The studies suggest that endogenous PGI2 production may play a role in bone metabolism, and it is possible that P GI2 release may be responsible for the frequent association between vascular invasion and resorption of bone or calcified cartilage in physiologic remodeling and pathologic osteolysis.

TL;DR: It is concluded that one of the reasons for the low incidence of myocardial infarction in Eskimos could be that the pro-aggregatory arachidonic acid is replaced in their phospholipids by the anti-aggRegatory EPA.

TL;DR: It is suggested that human endometrium and myometrium differ in their ability to metabolize arachidonic acid and in their inability to convert the endoperoxides formed, to PG's.

TL;DR: The results show that PGI2 prevents blockage of partially obstructed coronary arteries and this effect correlates with inhibition of platelet aggregation and the data suggest that locally produced P GI2 may have a local antiaggregatory effect without inhibiting platelet aggregating in the general circulation.

TL;DR: Antigen-antibody complexes (Ag/Ab) formed at equivalence stimulate the release of arachidonic acid and synthesis of prostaglandin E2 and 6-keto-prostaglandsin F1 alpha by resident mouse peritoneal macrophages.

TL;DR: The results suggest that thromboxanes and prostacyclin, as well as PGE2, contribute to the acute inflammatory response.

TL;DR: Pericardium, pleura and peritoneum form substantially high amounts of prostacyclin and HETE indicating that these tissues contain both cyclo-oxygenase and prostacyClin-synthetase, and they also show considerable lipoxygen enzyme activity.

TL;DR: Endogenously formed prostaglandins D2, E2 and F2 alpha were determined in homogenates of brain regions from rat, guinea-pig, rabbit and cat, using gas-chromatography-mass spectrometry.

TL;DR: Daily treatment with flurbiprofen starting before injection of the cancer cells reduced tumour growth and lengthened the survival of mice whose tumours were excised at 3 weeks.

TL;DR: Platelet THETE synthesis from arachidonate was not inhibited by preincubation with asprin or indomethacin but was blocked by 5,8,11,14-eicosatetraynoic acid, so THE appears to arise via the platelet lipoxygenase pathway rather than via the prostaglandin cyclooxygen enzyme.

TL;DR: Prostacyclin lowers the tonus and reduces the spontaneous motility of isolated pregnant human myometrium and seems to be related to coclic-AMP accumulation, since PGI2 increases the formation of this cyclic nucleotide in incubated minces of pregnant and non-pregnant uterus.

TL;DR: Tissues from human umbilical cord arteries and placental veins generated much greater prostacyclin activity than vessels from normal adults, which could contribute to maintaining the low peripheral vascular resistance typical of foetal circulation.

TL;DR: In 1 X 10(-5)M concentrations PGI2 contracted the arterial muscle and did not antagonize contractions induced by serotonin or PGF2 alpha, which supports the hypothesis that P GI2 is a mediator of vasodilatation.

TL;DR: This is the first demonstration of direct alteration of membrane components by a chemotactic agent and may be an example of a more generalized mechanism for altering membrane characteristics.

TL;DR: The hypothesis that prostaglandins are produced within the glomerulus where they may affect local glomerular blood flow and function is supported.

TL;DR: During ischemia following decapitation, instead, PGF2 alpha, and TXB2, show considerable increase, and levels of arachidonic acid metabolites are not modified.

TL;DR: It is concluded that, unless such a contamination can be monitored and corrected for, measurement of male U-PGE1 should be considered of questionable relevance to renal PG-synthesis.

TL;DR: Observations from rat basophilic leukemia cells strongly implicate the lipoxygenase pathway in slow reacting substance biosynthesis.

TL;DR: No obvious mechanisms for the actions of PGE2 or PGI2 were apparent although both agents lowered blood pressure and reduced the size of the occluded zone produced by ligation, which was more effective in this test situtation than dl-propranolol.

TL;DR: It is suggested that PGI2, if a significant renal prostaglandin, may modulate renal neuroeffector transmission post-junctionally, thereby forming a complement to the prejunctional action of PGE2.

TL;DR: In this paper, stable isotope dilution GC-MS was used to assess the 6-oxo-PGI2 hydration product in six normal volunteers infused with increasing doses of PGI2 intravenously.

TL;DR: The results indicate that the availability of precursor acids is one limiting factor in PG biosynthesis in rats, and small differences in the level of precursor acid, affected by dietary trans fatty acids may cause large variations in amounts of PGs synthesized.

TL;DR: It was concluded that the site of analgesic action of opioid-antagonists is peripheral rather than central, and agents derived from morphine, morphine-antagonist, enkephalins or cGMP devoid of central effect but having a strong peripheral effect may constitute a new class of safer analgesics.

TL;DR: The data support the hypothesis that the vasodilating effect of NIC is largely dependent upon an increased vascular formation of PG.

TL;DR: The omega-6 and omega-9 hydroperoxides of arachidonic acid caused dose-dependent constriction of cat coronary arteries and it is suggested that they have a direct effect on the arteries which can be antagonized by anti-inflammatory drugs.

TL;DR: During menstruation tolfenamic acid relieved endometriotic symptoms more effectively than placebo while indomethacin and acetylsalicylic acid did not differ from placebo.