Showing papers in "Prostaglandins in 1977"

TL;DR: A model of platelet homeostasis is proposed that suggests platelet aggregation is controlled by a balance between the adenylate cyclase stimulating activity of prostacyclin, and the cAMP lowering activity of PGH2.

TL;DR: Prostacyclin (PGX) strikingly increases cyclic AMP concentrations in human platelets, and these results correlate well with the anti-aggregating activity of prostacyClin, compared with PGE1 and PGD2.

TL;DR: Results strongly suggest that prostacyclin mediates the relaxation induced by arachidonic acid in bovine coronary artery strips, and is probably involved in the local regulation of the coronary vascular bed.

TL;DR: The hypothesis is advanced that certain prostaglandins may protect the mucosa ("cytoprotection") by preventing the spread of microorganisms and/or their toxin through the intestinal wall through the intestine wall.

TL;DR: Radiochemical data confirms that imidazole blocks the formation of 14C-thromboxane B2 from14C-PGH2 and could help to elucidate the role of thromboxanes in physiology or pathophysiology.

TL;DR: The wide occurrence of thromboxane and prostacyclin synthetases suggests that their biological roles are not limited to the cardiovascular system.

TL;DR: Results suggest that in atherosclerosis an impaired activity of the endothelial prostacyclin synthexizing system contributes to the intra-arterial formation of thrombi.

TL;DR: Intravenous injection of thromboxane A2 into anaesthetized quinea pigs was followed by a pronounced increase in the tracheal insufflation pressure, potency compared to prostaglandin H2, 31-45.

TL;DR: Results indicate that PGD2 is the major cyclooxygenase product in the central nervous system of the rat.

TL;DR: It is proposed that PGI2 exerts a direct effect on the release of renin from cortical cells and may be the mediator of arachidonate or prostaglandin endoperoxide stimulated renin secretion.

TL;DR: Progesterone concentrations were maintained in pregnant pigs and were indicative of luteal maintenance and systematic differences in day trends of utero-ovarian venous plasma estradiol were detected between O and P pigs.

TL;DR: Data indicate estradiol valerate may exert its luteotrophic effect by preventing PGF release from the uterus by preventing plasma steroid hormone concentrations in control and EV treated gilts.

TL;DR: The formation of prostaglandin D2 during platelet aggregation could represent a mechanism of feedback inhibition of aggregation, and was conclusively identified by gas chromatography-mass spectrometry.

TL;DR: Needleman et al. as mentioned in this paper showed that bradykinin effect on fatty acid release suggests that hormone stimulation either activates a specific lipase that distinguishes different fatty acids in the 2 position or activates lipase which is selectively compartmented with arachidonate-containing phospholipids.

TL;DR: In this paper, BHT, DL-α-tocopherol and Trolox C were shown to be non-specific inhibitors of both prostaglandin synthetase and soybean lipoxidase.

TL;DR: In this paper, the major prostaglandin (PG) biosynthesised by the ram seminal vesicle cyclo-oxygenase from arachidonic acid was 6-keto-PGF1α.

TL;DR: It is suggested that furosemide enhances urinary excretion of prostaglandin E by mechanisms which entails either an increase in prostaglandsin synthesis or a decrease in renal metabolism.

TL;DR: The results are consistent with the emerging hypothesis that PGE2 produced intrarenally plays a physiological role in natriuresis.

TL;DR: MIX inhibited effects of PGF2alpha on rat uterus and PGE1 on guinea pig ileum, and effective concentrations of theophylline were similar to the therapeutic levels in human plasma, suggesting that PGs may also be involved in regulating PDE action.

TL;DR: PGI2 was less active than PGE2 or PGF2alpha in contracting guinea-pig trachea and rat uterus; 6-oxo-PGF1alpha was active only on the rat uterus, and can be distinguished from the other stable prostaglandins using the cascade method of superfusion.

TL;DR: By utilizing albumin to trap released fatty acid, it was found that hormone-stimulated release of arachidonic acid is also transient, which directly demonstrates that tachyphylaxis occurs at a step prior to the cyclo-oxygenase.

TL;DR: Preliminary results suggest that a small fraction of the 3H-labled arachidonic acid which was taken up by these cells in vitro was associated with slow reacting substance, postulate that slow reacting substances of anaphylaxis may be derived from a prostaglandin endoperoxide which is formed during the oxidation of arachidsonic acid by the prostaglandsin fatty acid cyclooxygenase.

TL;DR: Since PGF2alpha can induce complete luteolysis it may be of use as an abortifacient in the bitch and dependent on a fall in progesterone, radioimmunoassayed in samples collected before, during, and after a 72 hr treatment period for Beagle bitches.

TL;DR: Increased cellular cAMP, induced by PGE 1, antagonizes the mobilization of the Ca 2+ which is normally required for PLA 2 activity, indicating that activation of PLA 2 can occur.

TL;DR: Prostaglandin D2 was shown to be more active than PGF2alpha in decreasing dynamic lung compliance, tidal volume, and expiratory airflow rate, as well as in elevating lung resistance, and potent biologic activity of PGD2 has been shown in the dog.

TL;DR: It is concluded that in advance atherosclerosis the platelet system is hypersensitive to biologically active metabolites of arachidonic acid.

TL;DR: Loperamide, a new antidiarrhoeal compound, effectively antagonised prostaglandin induced diarrhoea in adult healthy male volunteers and in patients undergoing pregnancy termination with prostag landins.

TL;DR: Ulastructural studies of the platelet response revealed that agents acting directly or indirectly to increase the level of cyclic AMP inhibited the action of arachidonic acid on washed platelets and prevented internal platelet contraction as well as aggregation.

TL;DR: The Prostaglandin-synthesis inhibitor: Naproxen-Sodium (NS) (an analgesic agent) very significantly reduced the "resting" and "active" pressures and the frequency of cyclic uterine activity of 10 dysmenorrheic patients.