Clinical pharmacokinetics of propofol given as a constant-rate infusion and in combination with epidural blockade

Wessén, Arne; Persson, Peter M.; Nilsson, Anders; Hartvig, Per

doi:10.1016/0952-8180(94)90058-2

Cited by 17 publications

(4 citation statements)

References 15 publications

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“…Epidural anesthesia has been reported as exerting no influence on the pharmacokinetics of propofol. 16 During clinical anesthesia, however, the decline of blood pressure with epidural block is frequently corrected by catecholamine infusion. This might produce a hyperdynamic state and bring about decreases in propofol concentration.…”

Section: Discussionmentioning

confidence: 99%

Une perfusion de dopamine diminue la concentration de propofol pendant le bloc péridural sous anesthésie générale

Takizawa

Nishikawa

Sato

et al. 2005

Can J Anesth/J Can Anesth

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P Pu ur rp po os se e: : It is common clinical practice to use dopamine to manage the reduction in blood pressure accompanying epidural blockade. As propofol is a high-clearance drug, propofol concentrations can be influenced by cardiac output (CO). The purpose of the present study was to investigate the effects of dopamine infusions on propofol concentrations administered by a target-controlled infusion system during epidural block under general anesthesia.

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Section: Discussionmentioning

confidence: 99%

Une perfusion de dopamine diminue la concentration de propofol pendant le bloc péridural sous anesthésie générale

Takizawa

Nishikawa

Sato

et al. 2005

Can J Anesth/J Can Anesth

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“…The major benefits of propofol are a rapid onset of action of < 3 minutes, and a short wash-out time due to its short half-life (1 to 2 hours after prolonged administration). 91 Propofol is a sedative-hypnotic agent with a diverse mechanism of action. It activates GABA A receptors directly, inhibits the NMDA receptor, and modulates calcium influx through slow calcium-ion channels.…”

Section: Refractory Convulsive Status Epilepticusmentioning

confidence: 99%

Seizures and Status Epilepticus in the Intensive Care Unit

Ziai

Kaplan²

2008

Semin Neurol

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Persistent seizures and failure to regain consciousness following witnessed seizure activity require emergency neurological consultation. Although outcome is largely dependent on underlying cause, early maximal anticonvulsant therapy is critical to reducing morbidity. This review covers important concepts in the clinical and EEG diagnosis of status epilepticus, and discusses treatment algorithms for single and recurrent seizures, emphasizing the need to rationalize therapy depending on the presumed duration of seizure activity. The review takes the perspective of the neurological consultant in the intensive care unit, and considers all pharmacological approaches available to the intensivist as described in the current literature and from clinical experience.

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“…Barbiturates also rapidly enter the brain in SE; however, the elimination half-life is about 100 h in phenobarbital [112] and 8 h after single-dose thiopental, increasing to 18 -36 h after prolonged treatment [113].The pharmacokinetic advantage of propofol is the rapid onset of action within minutes [112] and the rapid offset with an elimination half-life of 2 -3 h [114].…”

Section: Pharmacokinetics Of Gabaergic Anticonvulsantsmentioning

confidence: 99%

Anticonvulsant, antiepileptogenic, and antiictogenic pharmacostrategies

Holtkamp

Meierkord

2007

Cell. Mol. Life Sci.

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Pharmacological concepts tailored to status epilepticus, to epileptogenesis following acquired brain insults, and to ictogenesis in established epilepsy vary considerably and should ideally be directed at those pathophysiological mechanisms that presumably underly these conditions. Currently known important molecular targets include voltage-gated sodium and calcium channels, the gamma-aminobutyric acid (GABA) system and ionotropic glutamate receptors. Metabotropic glutamate receptors, potassium channels, and neurotransmitters such as acetylcholine, glycine, and monoamines are beyond the scope of this review. In status epilepticus, immediate failure of GABAergic inhibition occurs, and administration of benzodiazepines and barbiturates displays the pharmacostrategic mainstay. In epileptogenesis within limbic structures, the most important underlying pathophysiological mechanisms currently discussed are transient loss of inhibition and aberrant mossy fiber sprouting. Both processes may be facilitated by N-methy-D: -aspartat (NMDA) receptor regulation. NMDA antagonists may exhibit antiepileptogenic properties in experimental animals, but reliable data in humans are lacking. In established epilepsy, voltage-gated ion channels and impairment of GABAergic functions contribute to mechanisms facilitating ictogenesis. Blockade of sodium and calcium channels and enhancement of GABAergic inhibition are currently the most important tools to prevent the occurrence of seizures.

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Clinical pharmacokinetics of propofol given as a constant-rate infusion and in combination with epidural blockade

Cited by 17 publications

References 15 publications

Une perfusion de dopamine diminue la concentration de propofol pendant le bloc péridural sous anesthésie générale

Une perfusion de dopamine diminue la concentration de propofol pendant le bloc péridural sous anesthésie générale

Seizures and Status Epilepticus in the Intensive Care Unit

Anticonvulsant, antiepileptogenic, and antiictogenic pharmacostrategies

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