Prostaglandins and opioids.

In guinea-pig small intestine, rat brain in vitro and neuroblastomaXglioma hybrid cells, opioids specifically inhibit the action of E prostaglandins. In the whole rat, E prostaglandins, administered centrally, antagonize the antinociceptive action of morphine. E prostaglandins also antangonize the induction of opioid tolerant/dependence. In turn, tolerance/dependent preparations respond with added intensity to E prostaglandins. The antagonism between opioids and E prostaglandins does not occur at the opioid receptor; but, certainly in some preparations and probably in others, this antagonism occurs at the coupling or catalytic unit of a neuronal adenylate cyclase that opioids inhibit and E prostaglandins stimulate. The proposition that antagonism of E prostaglandin at appropriate neurons in the brain is part of the natural mechanism of opioid analgesia remains possible, but unproven, and is worth continued investigation.     

Prostaglandins in human seminal plasma. Prostaglandins and related factors 46

This study on human seminal plasma sought after the compounds which either possess the dienone chromophore or can be converted into it by treatment with sodium hydroxide. In addition, this investigation led to the isolation of 8 more (PGs) prostaglandins which were present in higher concentrations than the previously recognized PGs. Samples of human seminal plasma were subjected to silicic acid chromatography, reversed phase partition chromatography, thin layer chromatography, and gas liquid chromatography which isolated those 8 PGs not previously recognized. 4 of these compounds, PGE1-217, PGE2-217, PGE1-278, and PGE2-278 were known from earlier studies but had not been isolated from natural sources. The other 4 were 19 hydroxy derivatives of the 4 abovementioned compounds. The concentrations of the previously recognized PGs were recently determined and it was found that the 19 hydroxy derivatives were present in concentrations 4 times higher than the PGE compounds.     

Prostaglandins and premenstrual syndrome.

We examined plasma PGF2 alpha, PGE, PGE2, TXB2 and 6-keto-PGF1 alpha at intervals throughout 3 menstrual cycles in 20 patients with PMS. Similar measurements throughout 1 menstrual cycle were made in 12 age-matched control women. The plasma concentration of PGF2 alpha in the late luteal phase was significantly lower in patients with PMS compared with that in the control subjects. The plasma concentrations of PGE in the middle follicular phase and middle luteal phase, PGE2 alpha in the middle follicular phase and TXB2 in the middle and late luteal phase were significantly higher in 20 patients compared with the values in the controls. A disturbance of PG metabolism may contribute to the etiology of PMS.     

Pharmacological modification of thromboxane and prostaglandin release in cardiac anaphylaxis

Isolated perfused sensitized guinea pig hearts release relatively larhe amounts of radioimmunologically measurable thromboxane B₂ (TXB₂) as well as smaller amounts of prostaglandins (PGs) after antigenic challenge. Using thin layer chromatography the major PG released was shown to co-chromatograph with PGD₂, while smaller amounts of immunoreactive PGF_2α were found. The TX-synthetase inhibitor imidazole (100 μg/ml) significantly decreased TXB₂ release and simultaneously increased PG release during cardiac anaphylaxis. On the other hand, the β-sympathomimetic drug isoproterenol decreased both TXB₂ and PG release from the anaphylactic hearts. While isoproterenol significantly diminished anaphylactic coronary flow reduction, imidazole was without effect in this respect. PGD₂ (0.5 μ/min and 5.0 μg/min) infused intraaortally into non-sensitized guinea pig hearts reduced coronary flow dose-dependently. These results are compatible with the view that release of TX and PGs might contribute to coronary flow reduction in cardiac anaphylaxis.     

Prostaglandins in neural crest-tumors.

Prostaglandin and catecholamine concentrations were estimated in tumour tissues taken from four phaeochromcytomas and five other neural-crest tumours. Prostaglandins were found to be present in tumours both associated and non-associated with chronic diarrhoea. Prostaglandin F, as well as catecholamine, concentrations were higher in phaeochromocytomas than in other tumours. The hypothesis has been made that while prostaglandins do not reach arterial circulation to give rise to pharmacological effects, such as chronic diarrhoea, prostaglandins F present in phaeochromocytomas may contribute to a higher catecholamine synthesis and/or release, resulting in a higher incidence of hypertension associated with these tumours.