Dexmedetomidine Increases the Cocaine Seizure Threshold in Rats

Whittington, Robert A.; Virág, László; Vulliemoz, Yvonne; Cooper, Thomas B.; Morishima, Hisayo O.

doi:10.1097/00000542-200209000-00024

Cited by 55 publications

(38 citation statements)

References 17 publications

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“…Na anestesia geral, o problema mais freqüentemente observado Vol. 57 17,18 . A associação de cocaína, de infarto agudo do miocárdio (IAM) e de isquemia miocárdica foi primeiramente notada em 1982.…”

Section: Anestesiaunclassified

“…Fármacos, tradicionalmente considerados anticonvulsivantes, como os benzodiazepínicos, os barbitúricos, a fenitoína e os anestésicos inalatórios mostraram-se ineficazes em convulsões induzidas pela cocaína. As alterações fisiológicas relacionadas à cocaína podem ser tratadas com agonistas α 2 -adrenérgicos como a dexmedetomidina e a clonidina, com antagonistas α 1 periféricos, como a fentolamina, com hidratação e com benzodiazepínicos 18 . As complicações pulmonares secundárias ao uso da cocaí-na ocorrem em 25% dos usuários e se estendem desde crises de asma até hemorragias pulmonares fatais 34 .…”

Section: Anestesiaunclassified

“…Individuals admitted to emergency rooms with non-traumatic chest pain should be questioned about cocaine use. Aortic dissection and rupture, arrhythmias, myocarditis, and dilated cardiomyopathy should also be considered in patients complaining of thoracic pain 17,18 . The association of cocaine, myocardial infarction (MI), and myocardial ischemia was noticed initially in 1982.…”

Section: Anesthesiamentioning

confidence: 99%

“…Traditional antiseizure drugs, such as benzodiazepines, barbiturates, phenytoin, and inhalational anesthetics, have proved ineffective in the treatment of cocaine-induced seizures. The physiological changes related to cocaine can be treated with α 2 -adrenergic agonists, such as dexmedetomidine and clonidine, with peripheral α 1 -antagonists, such as phentolamine, with hydration, and with benzodiazepines 18 . Pulmonary complications secondary to cocaine use affect approximately 25% of the individuals, varying from asthma exacerbations to fatal pulmonary hemorrhage 34 .…”

Section: Anesthesiamentioning

confidence: 99%

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Anestesia no paciente usuário de cocaína

Luft

Mendes

2007

Rev. Bras. Anestesiol.

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RESUMOLuft A, Mendes FF -Anestesia no Paciente Usuário de Cocaína. JUSTIFICATIVA E OBJETIVOS:A cocaína é a droga ilícita mais freqüentemente associada a óbitos, e suas implicações perioperatórias nos pacientes agudamente intoxicados ou com história de uso crônico precisam ser bem conhecidas pelos anestesiologistas. O conhecimento da neurofisiologia, da farmacologia e das conseqüências fisiopatológicas decorrentes do uso da cocaína poderá facilitar o cuidado desses pacientes. O objetivo deste trabalho foi revisar as informações sobre a cocaína e suas interações com a anestesia. CONTEÚDO:O artigo discute a farmacologia da cocaína, as conseqüências fisiopatológicas decorrentes do seu uso e as interações com a anestesia. CONCLUSÕES:A compreensão e o reconhecimento precoce das complicações associadas ao uso de cocaína são essenciais para o manuseio adequado de pacientes usuários desta droga. O anestesiologista deve estar preparado, pois tanto as anestesias regionais quanto a geral apresentam riscos significativos nesses pacientes. Unitermos: COMPLICAÇÕES: drogas ilícitas; DROGAS: cocaína. SUMMARYLuft A, Mendes FF -Anesthesia in Cocaine Users. BACKGROUND AND OBJECTIVES:Cocaine is the illicit drug most frequently associated with death, and the anesthesiologist should be aware of the perioperative complications of this drug in patients with acute intoxication or with a history of chronic use. The knowledge of the neurophysiology, pharmacology, and physiopathological consequences of cocaine abuse may facilitate the care of these patients. The objective of this work was to review the information on cocaine and its interactions with anesthesia.CONTENTS: This paper discusses the pharmacology, physiopathological consequences of cocaine use, and its interactions with anesthesia. CONCLUSIONS:The knowledge and early recognition of the complications associated with the use of cocaine are essential for the adequate management of cocaine users. The anesthesiologist should be prepared because both regional and general anesthesia carry significant risks in those patients.

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Section: Anestesiaunclassified

Section: Anesthesiamentioning

confidence: 99%

Section: Anesthesiamentioning

confidence: 99%

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Anestesia no paciente usuário de cocaína

Luft

Mendes

2007

Rev. Bras. Anestesiol.

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“…Interestingly, overexpression of α 1B receptors was associated with spontaneous seizures in mutant animals [16], despite the fact that α 1 receptors generally have generally anticonvulsant properties [28,29]. α 2 receptor agonists also exert an anticonvulsant effects, particularly against pentylenetetrazol [24,26,20], kainic acid [2,8] and cocaine [30]. However, exogenously injected α 2 receptor agonists can act on neurons other than noradrenergic, such as dopaminergic or serotonergic neurons.…”

mentioning

confidence: 99%

Genetic deletion of the norepinephrine transporter decreases vulnerability to seizures

Kamiński

Shippenberg

Witkin

et al. 2005

Neuroscience Letters

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Norepinephrine (NE) has been reported to modulate neuronal excitability and act as endogenous anticonvulsant. In the present study we used NE transporter knock-out mice (NET-KO), which are characterized by high levels of extracellular NE, to investigate the role of endogenous NE in seizure susceptibility. Seizure thresholds for cocaine (i.p.), pentylenetetrazol (i.v.) and kainic acid (i.v.) were compared in NET-KO, heterozygous (NET-HT) and wild type (NET-WT) female mice. The doseresponse curve for cocaine-induced convulsions was significantly shifted to the right in NET-KO mice, indicating higher seizure thresholds. The threshold doses of pentylenetetrazol that induced clonic and tonic seizures were also significantly higher in NET-KO when compared to NET-WT mice. Similarly, NET-KO mice displayed higher resistance to convulsions engendered by kainic acid. For all drugs tested, the response of NET-HT mice was always intermediate. These data provide further support for a role of endogenous NE in the control of seizure susceptibility. KeywordsPentylenetetrazol; Kainic acid; Cocaine; Norepinephrine transporter; Seizures; Knock-out mice Norepinephrine (NE), released from neurons in the CNS, has been implicated in the modulation of seizure susceptibility. Inhibition of NE neurotransmission was reported to exacerbate seizures [5,21], while enhancement of NE neurotransmission appears to have anticonvulsant effects [18]. More recently, studies in mice lacking NE due to the genetic deletion of the enzyme dopamine beta-hydroxylase showed an increased susceptibility to seizures in the mutants [27] further supporting the hypothesis that NE might act as an endogenous modulator of convulsive seizures (for reviews see [28,7]). However, a fundamental question remains as to whether an elevation of extracellular levels of endogenous NE has an opposite effect. The recent generation of mice lacking the NE transporter (NET-KO), offered the opportunity to explore this question since extracellular NE levels are 100% higher in these animals compared to wild-type litter mates (NET-WT) [32]. Therefore, in the present study we have compared the susceptibility of NET-KO, heterozygous (NET-HT) and NET-WT mice to seizures induced by three distinct convulsant agents, i.e. cocaine, pentylenetetrazol and kainic acid.

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Sedation in the Intensive Care Unit: Challenges, Outcomes, and Future Strategies

Tobias

2011

Pediatric Sedation Outside of the Operating Room

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Dexmedetomidine Increases the Cocaine Seizure Threshold in Rats

Abstract: These data suggest that dexmedetomidine increases the cocaine-induced seizure threshold possibly a mechanism related to the attenuation of the extracellular dopaminergic neurotransmitter response to cocaine.

Cited by 55 publications

References 17 publications

Anestesia no paciente usuário de cocaína

Anestesia no paciente usuário de cocaína

Genetic deletion of the norepinephrine transporter decreases vulnerability to seizures

Sedation in the Intensive Care Unit: Challenges, Outcomes, and Future Strategies

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