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Cette seconde édition reprend largement les conclusions que nous avions évoquées et qui n'ont pas été démenties par les travaux ultérieurs. Les auteurs se sont efforcés de simplifier le plan de l'ouvrage, tout en visitant les domaines qui avaient été peu ou pas abordés : *le point sur l'utilisation de la kétamine en PCA ou par voie orale, *la découverte de propriétés antidépressives qui pourraient jouer un rôle dans l'analgésie des syndromes douloureux chroniques, *la toxicité possible, également, notamment sur l'appareil urinaire, de la kétamine utilisée au long cours dans le cadre de la douleur chronique, mais également chez les toxicomanes. De multiples exemples des concentrations plasmatiques attendues selon les doses et les modes d'administration ont également été fournis sous la forme de courbes obtenues par simulation, de façon à faire percevoir au lecteur les rapports entre l'utilisation pratique proposée et les effets cliniques, tant bénéfiques qu'indésirables, en particulier sur le plan psychique.
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Ketamine is an anesthetic synthetized for the first time in 1962, whose action mechanism depends on a non-competitive inhibition of the NMDA receptors. lts psychodysleptic effects led to the emergence of its recreational use. Although ketamine illicit use has never become comparable to that of the main recreational drugs in Europe, it expanded in Asia where ketamine has become the most abused drug.Although its use in clinical practice remains relatively safe, ketamine has shown certain toxicities among recreational users, in a chronic as well as acute way. The most obvious example of ketamine toxicity is its effect on urinary tract with the occurrence of ketamine induced cystitis, which was described for the first time in 2007.Ketamine toxicity also occurs on gastrointestinal, psychological and cognitive levels. People suffering from acute ketamine intoxication show various symptoms including cardiovascular issues, dizziness and altered levels of consciousness. The risk of death following overdose after the use of ketamine alone remains low, but users are at high risk of accident due to its analgesic and psychodysleptic effects.Recently, methoxetamine was advertised and marketed as a legal and "bladder friendly" alternative to ketamine. Actual researches give some indications that show that methoxetamine may have toxic effects similar to those of ketamine. Intoxications and death cases have already been reported. La kétamine est un agent anesthésique synthétisé pour la première fois en 1962, dont le mécanisme d'action dépend d'une inhibition non-compétitive des récepteurs NMDA. Ses propriétés psychodysleptiques particulières l'ont conduite à être détournée de son usage clinique afin d'être consommée pour des raisons récréatives. Bien que la consommation de kétamine n'ait jamais explosé en Europe par rapport aux autres drogues récréatives, la kétamine s'est largement répandue en Asie où elle est devenue la drogue la plus consommée.Bien que son utilisation dans la pratique clinique soit relativement sûre, la kétamine n'est pas dénuée de toxicité. Celle-ci se manifeste aussi bien de manière chronique qu'aigüe. 'exemple le plus évident de la toxicité de la kétamine est son effet délétère sur l'appareil urinaire et l'apparition de cystites induite> par la kétamine, une condition décrite pour la première fois en 2007. a toxicité de la kétamine se manifeste également au niveau gastro intestinal et sur les plans psychologiques et cognitifs. Les intoxications aigües à la kétamine se manifestent par des symptômes cardiovasculaires ainsi qu'une altération de la conscience et des vertiges. e risque de décès par overdose après ingestion de kétamine seule est faible, mais de par ses effets psychodysleptiques et analgésiques, la kétamine expose le consommateur à un haut risque d'accident.Récemment, la méthoxétamine a été présentée et vendue comme une alternative à la kétamine légale et non dangereuse pour la vessie. Les recherches effectuées actuellement laissent penser que sa toxicité urinaire serait similaire à celle de la kétamine, et des cas d'intoxication et de décès liés à la méthoxétamine ont déjà été rapportés.
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In the past, ketamine was considered a dangerous medication with the potential for abuse as a recreational drug. Healthcare providers were warned of its dangers and taught to fear its use. With this book, we hope to eliminate any fear and misgivings associated with this drug. It can be a useful medication in many situations, some of which we describe herein. This book discusses the use of ketamine in anesthesia, pain disorders, depression, palliative care, and trauma situations. It also examines ketamine usage in developing countries.
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In the past, ketamine was considered a dangerous medication with the potential for abuse as a recreational drug. Healthcare providers were warned of its dangers and taught to fear its use. With this book, we hope to eliminate any fear and misgivings associated with this drug. It can be a useful medication in many situations, some of which we describe herein. This book discusses the use of ketamine in anesthesia, pain disorders, depression, palliative care, and trauma situations. It also examines ketamine usage in developing countries.
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In the past, ketamine was considered a dangerous medication with the potential for abuse as a recreational drug. Healthcare providers were warned of its dangers and taught to fear its use. With this book, we hope to eliminate any fear and misgivings associated with this drug. It can be a useful medication in many situations, some of which we describe herein. This book discusses the use of ketamine in anesthesia, pain disorders, depression, palliative care, and trauma situations. It also examines ketamine usage in developing countries.
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Ketamine --- Analgesics --- Analgesia
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Ketamine and its mechanism of action are under control in their aenesthetic use but their antidepressant effect is not well known. However, recent studies are examining this characteristic so as to treat major nervous breakd owns.Research has shown a double link between, on the one hand depression and brain structure and on the other, between depression and a decrease in the functioning connected with neuroplasticity. But this neuroplasticity is, among others, influenced by neurogenesis and synaptogenesis. The glutamatergic way could favour the process of neuronal and synapticregulation through the neurotrophic factor (BDN F). At the same time it helps reduce the depression phenomenon.Recent studies have shown that ketamine could be a quick antidepressant solution among patients that resist standard treatments. Moreover, it has shown a decrease in suicidai thoughts. Ketamine would quickly reverse the synaptic deficit blocking the NMDA receptors.It would help release BDNF, which would activate the signalling path of mTOR and increase synaptogenesis. This way of treating depression seems promising but also raises major criticism. The hyperactivity of mTOR is mentioned in sorne cases of cancer. The use of ketamine remains difficult through its psychotornimetic effects and its repeated use asks for caution...new research is necessary. La kétamine et son mécanisme d'action, s'ils sont maîtrisés dans leur utilisation anesthésique, sont méconnus quant à leur effet antidépresseur. Pourtant des études récentes examinent cette particularité afin de traiter les dépressions majeures.Les recherches ont démontré un double lien entre d'une part , la dépression et la structure cérébrale, et d'autre part entre la dépression et une diminution du fonctionnement lié à la neuroplasticité. Or, celle-ci est notamment influencée par la neurogenèse et la synaptogenèse. La voie glutamatergique pourrait favoriser les processus de régulation neuronale et synaptique via le facteur neurotrophique BDNF. Ce faisant, les symptômes dépressifs iraient en régressant. Des études récentes ont montré que la kétamine pouvait induire une réponse antidépressive rapide chez des patients résistant aux traitements standards. De plus elle a montré une diminution des idées suicidaires. La kétamine renverserait le déficit synaptique rapidement grâce à son blocage des récepteurs NMDA . Elle provoquerait la libération de BDNF qui activerait la voie de signalisation de mTOR et augmenterait la synaptogenèse.Cette façon de traiter la dépression, semble prometteuse mais suscite aussi des critiques majeures. L'hyperactivité de mTOR est signalée dans certains cas de cancers. L'utilisation de la kétamine reste difficile par ses effets psychotomimétiques et son utilisation répétée suscite la prudence ... de nouvelles recherches sont nécessaires.
Ketamine --- Depression --- Depressive Disorder
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In the past, ketamine was considered a dangerous medication with the potential for abuse as a recreational drug. Healthcare providers were warned of its dangers and taught to fear its use. With this book, we hope to eliminate any fear and misgivings associated with this drug. It can be a useful medication in many situations, some of which we describe herein. This book discusses the use of ketamine in anesthesia, pain disorders, depression, palliative care, and trauma situations. It also examines ketamine usage in developing countries.
Ketamine. --- Amines --- Anesthesia adjuvants --- Chlorobenzene --- Hexane
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Since the beginning of their use, 150 years ago, general anesthetics are used usually although their mechanisms of action are not exactly know. With current technology, an important step has been done in their understanding. With this, there is an increasing safety in their use. Indeed, we know the involvement of receptors such as GABA, NMDA receptors, ... as the center of the effect of general anesthetics. However, it remains, at present, many unanswered questions ... This work synthesizes the knowledge on this subject Depuis le début de leur utilisation, il y a 150 ans, les anesthésiques généraux sont utilisés couramment, alors que l’on ne connait pas exactement tous les mécanismes d’actions. Grâce aux techniques actuelles, un grand pas dans la compréhension de leurs fonctionnements a été franchi. Ce qui a permis d’augmenter grandement la sécurité de leur utilisation. En effet, on sait maintenant l’implication de récepteurs tels que le GABA, les récepteurs NMDA, … comme étant au centre de l’effet des anesthésiques généraux. Cependant, il reste encore, à l’heure actuelle, beaucoup de questions sans réponse… Ce travail synthétise l’essentiel des connaissances sur le sujet
Anesthetics, General --- Nitrous Oxide --- Halogens --- Propofol --- Ketamine --- Analgesics, Opioid
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The purpose of this collection is to provide a forum to integrate pre-clinical and clinical investigations regarding the long-term consequences of adolescent exposure to drugs of abuse. Adolescence is characterized by numerous behavioral and biological changes, including substantial neurodevelopment. Behaviorally, adolescents are more likely to engage in risky activities and make impulsive decisions. As such, the majority of substance use begins in adolescence, and an earlier age of onset of use (<15 yr) is strongly associated with the risk for developing a substance use disorder later in life. Furthermore, adolescent drug use may negatively impact ongoing neurological development, which could lead to long-term cognitive and emotional deficits. A large number of clinical studies have investigated both the acute and long-term effects of adolescent drug use on functional outcomes. However, the clinical literature contains many conflicting findings, and is often hampered by the inability to know if functional differences existed prior to drug use. Moreover, in human populations it is often very difficult to control for the numerous types of drugs, doses, and combinations used, not to mention the many other environmental factors that may influence adult behavior. Therefore, an increase in the number of carefully controlled studies using relevant animal models has the potential to clarify which adolescent experiences, particularly what drugs used when, have long-term negative consequences. Despite the advantages of animal model systems in clarifying these issues, the majority of pre-clinical addiction research over the past 50+ years has been conducted in adult animals. Moreover, few addiction-related studies have investigated the long-term neurocognitive consequences of drug exposure at any age. In the past 10 years of so, however, the field of adolescent drug abuse research has burgeoned. To date, the majority of this research has focused on adolescent alcohol exposure using a variety of animal models. The results have given the field important insight into why adolescents are more likely to drink alcohol to excess relative to adults, and the danger of adolescent alcohol use (e.g., in leading to a persistence of excessive drinking in adulthood). More recently, research regarding the effects of adolescent exposure to other drugs of abuse, including nicotine, cocaine, and cannabinoids has expanded. Therefore, we are at unique point in time, when emerging results from carefully controlled pre-clinical studies can inform the sometimes confusing clinical literature. In addition, we expect an influx of prospective clinical studies in response to a cross-institute initiative at NIH, known as the ABCD grant. Several institutes are enrolling children prior to adolescence (and the initiation of drug use), in order to control for pre-existing neurobiological and neurobehavioral differences and to monitor the age of initiation and amount of drug used more carefully than is possible using retrospective designs.
alcohol --- stress --- nicotine --- cocaine --- ketamine --- methamphetamine --- cannabinoid --- prefrontal cortex --- juvenile --- sex differences --- alcohol --- stress --- nicotine --- cocaine --- ketamine --- methamphetamine --- cannabinoid --- prefrontal cortex --- juvenile --- sex differences
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