33 research outputs found

    Hemorrhagic infarct of basal ganglia in cardiac arrest. CT and MRI findings. 2 cases

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    We report the CT and MRI findings in two cases of hemorrhagic infarct of the basal ganglia (BG), following out-of-hospital cardiac arrest (CA). In case 1, Brain-CT realized at day 2 showed bilateral and almost symmetric hemorrhagic infarct of the BG and infarct of the tectum of the mesencephalon. In case 2, MRI realized at day 6 showed hemorrhagic infarct of both lenticular nuclei on T2 GE images. In both cases there was no medical history and the cardiovascular and the coagulation profile were normal. In these cases, the lesions are observed earlier than reported in a few previous radiological cases. Similar lesions have been reported in pathological studies. These lesions seem occur early after CA. Reperfusion is probably responsible for the hemorrhagic transformation. The reason why some patients present either BG or brainstem infarct or both remains unclear. Bilateral and symmetric hemorrhagic infarct of the BG, especially of the Lenticular nuclei, and infarct of the dorsal pons and mesencephalic tegmentum seem to be a characteristic feature of profound and prolonged hypotension or of CA

    Clinical review: Aggressive management and extracorporeal support for drug-induced cardiotoxicity

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    Poisoning may induce failure in multiple organs, leading to death. Supportive treatments and supplementation of failing organs are usually efficient. In contrast, the usefulness of cardiopulmonary bypass in drug-induced shock remains a matter of debate. The majority of deaths results from poisoning with membrane stabilising agents and calcium channel blockers. There is a need for more aggressive treatment in patients not responding to conventional treatments. The development of new antidotes is limited. In contrast, experimental studies support the hypothesis that cardiopulmonary bypass is life-saving. A review of the literature shows that cardiopulmonary bypass of the poisoned heart is feasible. The largest experience has resulted from the use of peripheral cardiopulmonary bypass. However, a literature review does not allow any conclusions regarding the efficiency and indications for this invasive method. Indeed, the majority of reports are single cases, with only one series of seven patients. Appealing results suggest that further studies are needed. Determination of prognostic factors predictive of refractoriness to conventional treatment for cardiotoxic poisonings is mandatory. These prognostic factors are specific for a toxicant or a class of toxicants. Knowledge of them will result in clarification of the indications for cardiopulmonary bypass in poisonings

    Difficulties in assessing cytomegalovirus-associated gastric perforation in an HIV-infected patient

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    BACKGROUND: Active Cytomegalovirus (CMV) infection is a common complication in advanced symptomatic Human Immunodeficiency Virus (HIV) infection. CMV-induced intestinal perforations are hard to diagnose and may be observed throughout the gastrointestinal tract. Isolated stomach perforation is exceptional. CASE PRESENTATION: A 47-year-old man was admitted to our intensive care unit with multiorgan failure. Gastrointestinal endoscopic examination showed erythematous gastritis but normal duodenum and colon. CMV blood culture was positive. Histologic examination of a gastric biopsy showed inflammatory infiltrate and immunostaining typical intranuclear CMV inclusion bodies. Concomitant abdominal CT scan disclosed large peripancreatic hypodensities without pneumoperitoneum. The patient died despite supportive therapies and ganciclovir infusion. Postmortem examination showed a 4-cm gastric perforation adhering to the transverse colon and liver, with a thick necrotic inflammatory coating around the pancreas. The whole GI tract, except the stomach, was normal. As other causes, especially Helicobacter pylori infection could be ruled out, a causal relationship between CMV and gastric disease was assumed. CONCLUSION: CMV may be responsible for gastric perforations, with difficulties in assessing the diagnosis. Early diagnosis based on cautious endoscopy and histopathologic examination is needed to make a favorable outcome possible

    Antenatal glucocorticoid treatment induces adaptations in adult midbrain dopamine neurons, which underpin sexually dimorphic behavioral resilience

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    We demonstrated previously that antenatal glucocorticoid treatment (AGT, gestational days 16-19) altered the size and organization of the adult rat midbrain dopaminergic (DA) populations. Here we investigated the consequences of these AGT-induced cytoarchitectural disturbances on indices of DA function in adult rats. We show that in adulthood, enrichment of striatal DA fiber density paralleled AGT-induced increases in the numbers of midbrain DA neurons, which retained normal basal electrophysiological properties. This was co-incident with changes in (i) striatal D2-type receptor levels (increased, both sexes); (ii) D1-type receptor levels (males decreased; females increased); (iii) DA transporter levels (males increased; females decreased) in striatal regions; and (iv) amphetamine-induced mesolimbic DA release (males increased; females decreased). However, despite these profound, sexually dimorphic changes in markers of DA neurotransmission, in-utero glucocorticoid overexposure had a modest or no effect on a range of conditioned and unconditioned appetitive behaviors known to depend on mesolimbic DA activity. These findings provide empirical evidence for enduring AGT-induced adaptive mechanisms within the midbrain DA circuitry, which preserve some, but not all, functions, thereby casting further light on the vulnerability of these systems to environmental perturbations. Furthermore, they demonstrate these effects are achieved by different, often opponent, adaptive mechanisms in males and females, with translational implications for sex biases commonly found in midbrain DA-associated disorders

    Origine muscarinique centrale des effets ventilatoires du dichlorvos à dose toxique chez le rat

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    Objectif : Les organophosphorés sont fréquemment impliqués dans des intoxications chez l’homme. Leur toxicité se manifeste essentiellement sur le plan respiratoire. Des articles récents ont montré que la gravité de l’intoxication est dépendante de l’organophosphoré. Le but de ce travail est de comparer les effets ventilatoire du dichlorvos à ceux du diéthylparaoxon et de préciser leur origine. Méthodes : Les rats males Sprague-Dawley (n = 6) ont reçu en sous-cutanée le dichlorvos à la dose de 5,76 mg/kg. Au maximum des effets ventilatoires, les animaux ont reçu par voie intramusculaire 10 mg/kg d’atropine base ou une dose équimolaire de 5,42 mg/kg, méthylatropine base. Les effets ventilatoires sont mesurés par pléthysmographie corps entier chez l’animal vigile et la température centrale par télémétrie infrarouge. Résultats : Le dichlorvos induit rapidement des signes cliniques, une hypothermie maximale à 60 min, une baisse significative de la fréquence respiratoire résultant d’une augmentation du temps expiratoire et à une augmentation non significative du volume courant. Ces effets sont maximaux 5 min après l’injection et spontanément réversibles en 60 min. L’atropine corrige partiellement l’hypothermie, totalement les effets ventilatoires. La méthylatropine est sans effet sur le plan clinique, majore l’hypothermie et certains effets ventilatoires. Conclusion : Les effets ventilatoire induits par le dichlorvos sont comparables à ceux rapportés pour le diéthylparaoxon. Ils en diffèrent par des cinétiques d’apparition et de correction très rapides. L’atropine permet une correction complète de ces effets. L’inefficacité de la méthylatropine prouve que les effets ventilatoires ont une origine muscarinique purement centrale. and diethylparaoxon are similar. In contrast with diethylparaoxon, dichlorvos induced the rapid onset of short-lasting respiratory toxicity. Atropine completely reversed dichlorvos-induced respiratory toxicity while an equimolar dose of methylatropine was devoid of any effects evidencing the central muscarinic origin of respiratory toxicity

    Stratégies analytiques en toxicologie d'urgence

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    La Toxicologie d'urgence associe la notion d'exploration d'un très vaste domaine de substances chimiques à la notion d'efficacité de prise en charge thérapeutique du sujet intoxiqué. En conséquence, la stratégie analytique à adopter sera le fruit d'une collaboration clinico-biologique étroite comprenant l'approche clinique (anamnèse, signes cliniques), l'approche biologique (gazométrie, osmolalité, ionogramme, ...) et la connaissance des limites et des intérêts des différentes méthodes disponibles localement. Les méthodes spectrophotométriques et immunologiques sont des méthodes de dépistage au champ d'application limité et dont l'intérêt est d'apporter rapidement une orientation sur l'origine de l'intoxication (pesticides, médicaments, substances illicites, ...). Les méthodes séparatives associées à des outils de détection (spectres UV, spectres de masse) sont le complément indispensable à l'identification des molécules responsables de l'intoxication. En dernière étape, l'analyse quantitative du produit toxique identifié peut faire appel à une méthode immunologique (paracetamol, digoxine, ...) ou chromatographique (méprobamate, colchicine, ...)

    Comparison of the Respiratory Toxicity and Total Cholinesterase Activities in Dimethyl Versus Diethyl Paraoxon-Poisoned Rats

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    The chemical structure of organophosphate compounds (OPs) is a well-known factor which modifies the acute toxicity of these compounds. We compared ventilation at rest and cholinesterase activities in male Sprague-Dawley rats poisoned with dimethyl paraoxon (DMPO) and diethyl paraoxon (DEPO) at a subcutaneous dose corresponding to 50% of the median lethal dose (MLD). Ventilation at rest was recorded by whole body plethysmography. Total cholinesterase activities were determined by radiometric assay. Both organophosphates decreased significantly the respiratory rate, resulting from an increase in expiratory time. Dimethyl-induced respiratory toxicity spontaneously reversed within 120 min post-injection. Diethyl-induced respiratory toxicity was long-lasting, more than 180 min post-injection. Both organophosphates decreased cholinesterase activities from 10 to 180 min post-injection with the same degree of inhibition of total cholinesterase within an onset at the same times after injection. There were no significant differences in residual cholinesterase activities between dimethyl and diethyl paraoxon groups at any time. The structure of the alkoxy-group is a determinant factor of the late phase of poisoning, conditioning duration of toxicity without significant effects on the magnitude of alteration of respiratory parameters. For same duration and magnitude of cholinesterase inhibition, there was a strong discrepancy in the time-course of effects between the two compounds

    Influence du site de prélèvement sur l’étude cinétique et métabolique de l’éthanol

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    Objectif : L’analyste n’obtenant pas toujours les mêmes prélèvements sanguins, nous proposons d’étudier l’influence du site de prélèvement sanguin sur l’étude cinétique et métabolique de l’éthanol. Méthode : Sur un modèle animal, le rat mâle Sprague-Dawley âgé de 7 à 9 semaines, les cinétiques sanguines de l’éthanol, sériques de l’acétate et du lactate, artérielles et veineuses, sont déterminées respectivement par analyse de l’espace de tête en chromatographie en phase gazeuse et électrophorèse capillaire de zone. L’animal est cathétérisé soit au niveau d’une artère fémorale, soit au niveau d’une veine caudale. Résultats : Lors de la phase d’absorption, l’éthanolémie artérielle croît plus rapidement et plus intensément que l’éthanolémie veineuse; après la phase de distribution, elles tendent à se confondre. Contemporainement, les acétates, métabolites de l’éthanol, apparaissent plus concentrés dans le compartiment artériel que veineux périphérique; les lactates, produits indirects du métabolisme de l’éthanol, présentent une cinétique artérielle similaire à celle de l’acétate, les concentrations veineuses restant anormalement élevées pendant l’étude. Conclusion : Le sang veineux prélevé lors de cette étude n’a pas donné accès à la réalité cinétique et métabolique de l’éthanol. Ainsi, en comparaison avec le compartiment artériel, l’éthanol et l’acétate sont présents en quantité moindre dans le sang veineux, l’éthanol y apparaissant plus lentement. Le sang veineux prélevé s’est même avéré inadapté à l’étude cinétique des lactates. Cette étude confirme, si nécessaire, que les résultats et l’interprétation d’une analyse sont préconditionnés par le prélèvement lui-même, ce dernier n’étant pas toujours réalisé sous les indications d’un analyste
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