[Neuroimaging findings in eclamptic patients still symptomatic after 24 hours: a descriptive study about 19 cases]. / Apport de l'imagerie neurologique chez les éclamptiques encore symptomatiques après 24 heures: étude descriptive à propos de 19 cas.

OBJECTIVE: To describe the neuroimaging findings in eclamptic patients still symptomatic after 24 hours. PATIENTS AND METHODS: All parturients consecutively admitted over a 12-month period for eclampsia and presenting with neurological disorders (coma, focal neurological abnormalities, and eye sight disturbance) underwent cerebral CT-scan and/or MRI. RESULTS: Nineteen women were studied, and all had abnormal neuroradiological findings. The CT-scan was normal in three cases. Cerebral oedema was the predominant lesion (14 cases). It was localized in the parietal or occipital area (12 cases), paraventricular area (1 case), or was diffuse (1 case). Diffusion weighted MRI was performed in four cases and showed cytotoxic cerebral oedema in one case. There were three cases of cerebral venous thrombosis and two cases of intracerebral haemorrhage. CONCLUSION: Various neuroradiological lesions can be observed in eclamptic patients. A localized cerebral oedema is the most frequent. Diffusion weighted MRI should be systematically done when neurological disorders persist.

Highly sensitive immuno-assays for the determination of cotinine in serum and saliva. Comparison between RIA and an avidin-biotin ELISA.

Two immuno-assay methods (RIA and ELISA) have been developed for the accurate and sensitive measurement of cotinine in human body fluids (serum, saliva). RIA uses [3H]cotinine as antigen and charcoal/dextran for separating cotinine-bound antibodies from the free derivative. Another technique (ELISA) was developed to avoid the use of radio-labelled compounds and to determine cotinine in large populations, including passive or non-smokers who usually present very low concentrations. The two techniques were analytically validated. The detection limit was similar (0.1 micrograms/l) and the precision was better than 10% for both techniques. Non-smoker values ranged from 0.1 to 17 micrograms/l by ELISA and 0.1 to 27.5 micrograms/l by RIA, whereas smoker values ranged from 50 to 1000 micrograms/l (ELISA) and from 70 to 800 micrograms/l (RIA). The comparative analysis of cotinine in 96 human sera revealed a good correlation between the two methods (r = 0.97) and a reliable discrimination between the populations of non-smokers and smokers. As usual, the ELISA is more rapid (4 h 30 min) than the RIA (longer than 48 h). ELISA is proposed for use in the epidemiological investigation of the human tobacco risk.

A functional response to D1 dopamine receptor stimulation in the central nervous system: inhibition of the release of [3H]-serotonin from the rat substantia nigra.

The influence of dopamine receptor agonists on the calcium dependent electrically-evoked release of [3H]-serotonin was studied in the superfused rat substantia nigra. The electrically-evoked overflow of [3H]-serotonin was significantly inhibited by micromolar concentrations of exogenous dopamine and of the D1-selective dopamine receptor agonists, fenoldopam and SKF 38393. The inhibitory effects of dopamine and fenoldopam on [3H]-serotonin release were antagonized by the D1-selective dopamine receptor antagonist SCH 23390. S-sulpiride, an antagonist of D2 receptors failed to antagonize the inhibitory effects of dopamine on [3H]-serotonin release. Moreover, quinperol, the selective D2 receptor agonist did not modify the electrically evoked release of [3H]-serotonin. In the presence of nomifensine, SCH 23390 but not S-sulpiride enhanced in a concentration dependent manner the electrically-evoked release of [3H]-serotonin. Under similar experimental conditions, exposure to fenoldopam did not inhibit the electrically-evoked release of [3H]-serotonin from rat hippocampal or hypothalamic slices. These results indicate that, in rat substantia nigra, exogenous as well as endogenous dopamine causes inhibition of serotonin release by activation of dopamine receptors of the D1-subtype.

Newly synthesized noradrenaline mediates the alpha 2-adrenoceptor inhibition of [3H]5-hydroxytryptamine release induced by beta-phenylethylamine in rat hippocampal slices.

In slices of the rat hippocampus, alpha 2-adrenoceptors located presynaptically on serotonergic nerve terminals modulate the electrically evoked calcium-dependent release of [3H]serotonin [( 3H]5HT). We have investigated the effects of a naturally occurring trace amine, beta-phenylethylamine (beta-PEA), on noradrenergic transmission in the rat hippocampus. Under experimental conditions in which MAO of type B is inhibited by deprenyl-exposure to beta-PEA (0.1-10 microM) facilitates the spontaneous outflow of [3H]noradrenaline and inhibits the electrically evoked release of [3H]5HT. The inhibitory effect of beta-PEA (3 microM) on the evoked release of [3H]5HT was antagonized by the alpha 2-adrenoceptor antagonist idazoxan at 1 microM, and by pretreatment with alpha-methyl-p-tyrosine (alpha-MpT, 300 mg/kg i.p., 2 h). The inhibition of tyrosine hydroxylase activity by alpha-MpT does not modify the inhibition of the evoked release of [3H]5HT by the alpha 2-adrenoceptor agonist, 6-fluoronoradrenaline, or the serotonin receptor agonist, 5-methoxytryptamine. Pretreatment with the neurotoxin DSP4 (50 mg/kg i.p., 10 days) markedly antagonized the inhibitory action of beta-PEA on [3H]5HT release. These results indicate that the noradrenaline-releasing action of beta-PEA inhibits the electrically evoked release of [3H]5HT through the activation of alpha 2-adrenoceptors. This inhibitory effect appears to be mediated exclusively through the release of newly synthesized noradrenaline, and does not involve the direct activation by beta-PEA of the inhibitory 5HT autoreceptors which modulate [3H]5HT release in the rat hippocampus.

Phenylethylamine-induced release of noradrenaline fails to stimulate alpha 1-adrenoceptors modulating [3H]-acetylcholine release in rat atria, but activates alpha 2-adrenoceptors modulating [3H]-serotonin release in the hippocampus.

The modulation of the depolarization induced release of [3H]-acetylcholine by agonists acting on alpha-adrenoceptors was studied in superfused rat atrial slices. In this model, noradrenaline and methoxamine, but not UK 14304 reduced the potassium evoked release of [3H]-acetylcholine. The inhibitory action of these drugs was antagonized by the alpha 1 selective adrenoceptor antagonist prazosin. Propranolol, idazoxan and sulpiride did not antagonize the inhibition by noradrenaline of the potassium-evoked release of [3H]-acetylcholine. Exposure to amphetamine, beta-phenylethylamine, m- or p-tyramine, increased in a concentration-dependent manner the spontaneous outflow of [3H]-noradrenaline from atrial slices. Yet, these concentrations of the indirectly acting sympathomimetic amines, tested in the presence of an inhibitor of monoamine oxidase (MAO), failed to modify the potassium evoked release of [3H]-acetylcholine. Desipramine 3 mumol/l or cocaine 10 mumol/l did not affect the release of [3H]-acetylcholine evoked by potassium stimulation. Under similar experimental conditions, beta-phenylethylamine facilitated the spontaneous outflow of [3H]-noradrenaline, and inhibited the electrically-evoked release of [3H]-serotonin from the hippocampus by activation of alpha 2-adrenoceptors. It is concluded that the release of acetylcholine from atrial cholinergic neurons can be modulated through inhibitory alpha 1-adrenoceptors, which are not activated when the release of noradrenaline is induced by indirectly acting sympathomimetic amines. In addition, amphetamine or structurally related amines do not activate directly recognition sites in the cholinergic postganglionic parasympathetic neuron to modify the release of [3H]-acetylcholine.

Multiple high affinity binding sites for 5-hydroxytryptamine: a new class of sites distinct from 5-HT1 and S2.

Two different classes of binding sites probably related to serotonergic receptors have already been reported: 5-HT1 binding sites recognize [3H]5-hydroxytryptamine with a high affinity (Kd = 3 nM) and S2 binding sites recognize [3H]spiroperidol and [3H]ketanserine. An additional population of sites has been observed in crude membrane preparations or fractions enriched with synaptosomal membranes obtained from rat brain cortex. This population was observed as a single class of sites in a synaptosomal fraction (L fraction--according to Laduron (1977)). It corresponded to a dissociation constant Kd = 13-15 nM, and Bmax = 0.80 +/- 0.15 pmol/mg protein. Displacement experiments showed that it recognized preferentially the 5-HT structure (bufotenin, 5-MeO-tryptamine). Tryptamine was a weak displacer and 5,7-dihydroxytryptamine totally inefficient. Neither 8-OH-DPAT, nor quipazine had any effect. Methiothepin, cinanserin and cyproheptadine displaced 5-HT from these sites whereas ergot derivatives did not. Contrary to 5-HT1 binding, this recently observed binding was not altered by GTP; alpha-MSH reduced the corresponding Bmax whereas Leu-enkephalin did not. The degenerative lesion of the serotonergic fibers led to a slight increase in the Bmax of the binding without altering the Kd which means that corresponding sites are not located on serotonergic fibers and might be postsynaptically located.