Cerebrospinal fluid concentrations of atracurium, laudanosine and vecuronium following clinical subarachnoid hemorrhage

Tassonyi, E.; Fathi, Marc; Hughes, Garland; Chiodini, Florence; Bertrand, Daniel; Michelet, Dominique; Fuchs‐Buder, Thomas

doi:10.1034/j.1399-6576.2002.461011.x

Cited by 26 publications

(10 citation statements)

References 32 publications

(38 reference statements)

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“…However, there is evidence that patients with an impaired BBB function treated with either of these compounds, present autonomic dysfunction, seizures 39 and neuronal cell death 15. Furthermore, ROC, but not VEC, has been detected in cerebrospinal fluid in patients with subarachnoid haemorrhage who underwent neurosurgery 39,40,41. This finding could be attributed to the fact that ROC is more hydrosoluble than VEC, so it may easily arrives to central nervous system when BBB is damaged 42.…”

Section: Discussionmentioning

confidence: 99%

Neuronal Effects of Sugammadex in combination with Rocuronium or Vecuronium

Aldasoro¹,

Vallés²,

Aldasoro

et al. 2017

Int. J. Med. Sci.

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Rocuronium (ROC) and Vecuronium (VEC) are the most currently used steroidal non-depolarizing neuromuscular blocking (MNB) agents. Sugammadex (SUG) rapidly reverses steroidal NMB agents after anaesthesia. The present study was conducted in order to evaluate neuronal effects of SUG alone and in combination with both ROC and VEC. Using MTT, CASP-3 activity and Western-blot we determined the toxicity of SUG, ROC or VEC in neurons in primary culture. SUG induces apoptosis/necrosis in neurons in primary culture and increases cytochrome C (CytC), apoptosis-inducing factor (AIF), Smac/Diablo and Caspase 3 (CASP-3) protein expression. Our results also demonstrated that both ROC and VEC prevent these SUG effects. The protective role of both ROC and VEC could be explained by the fact that SUG encapsulates NMB drugs. In BBB impaired conditions it would be desirable to control SUG doses to prevent the excess of free SUG in plasma that may induce neuronal damage. A balance between SUG, ROC or VEC would be necessary to prevent the risk of cell damage.

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Section: Discussionmentioning

confidence: 99%

Neuronal Effects of Sugammadex in combination with Rocuronium or Vecuronium

Aldasoro¹,

Vallés²,

Aldasoro

et al. 2017

Int. J. Med. Sci.

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“…Seizures occur in animals at laudanosine cerebrospinal fluid (CSF) concentrations, approximately 100-1000-fold higher than in clinical conditions during general anesthesia. 15 Moreover, at concentrations comparable to those measured in CSF during and up to eight hours after anesthesia (14-38 ng/mL), namely at nM concentrations, laudanosine can activate a4b2 nACh subtype receptors (nAChRs). 15 Recent research showed that a4b2 receptors represent a primary molecular target for neuroprotection, 16 and activation of a4b2 nAChRs provided neuroprotection against NMDA excitotoxic cascade in a neonatal model.…”

Section: In Replymentioning

confidence: 95%

“…15 Moreover, at concentrations comparable to those measured in CSF during and up to eight hours after anesthesia (14-38 ng/mL), namely at nM concentrations, laudanosine can activate a4b2 nACh subtype receptors (nAChRs). 15 Recent research showed that a4b2 receptors represent a primary molecular target for neuroprotection, 16 and activation of a4b2 nAChRs provided neuroprotection against NMDA excitotoxic cascade in a neonatal model. 17 These finding are also consistent with another recent report in which nicotinic neuroprotection against excitotoxic effects of NMDA is initiated by direct activation of a4b2, or indirectly by inhibition of a7 nAChRs followed by signal transduction involving tyrosine kinases, phospholipid-dependent kinases and mitogen activated kinases.…”

Section: In Replymentioning

confidence: 95%

In reply

Fodale

Praticò

Leto

et al. 2005

International Journal of Obstetric Anesthesia

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With the stated dose (0.1 mg/kg) either it must have been necessary to assist ventilation to avoid desaturation while awaiting onset of adequate block for intubation, or intubation was performed without delay under conditions facilitated by the propofol bolus. I would regard neither approach as ideal in the obstetric patient.Although the authors wrote that neostigmine Ô2 mL' was given, I presume they meant 2 mg. Train-of-four neuromuscular stimulation was used, but, crucially, there is no documentation of a response (i.e. four twitches and absence of fade) that demonstrated complete reversal of neuromuscular block. I would be grateful if the authors would justify their choice of cisatracurium, and reassure me that their patients were fully reversed before extubation and the subsequent development of laryngospasm.

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“…Increased glutamate levels in brain microdialysate are associated with cognitive decline in preclinical models of circulatory arrest. Actracurium and its metabolite laudanosine activate α4β2 nicotinic acetylcholine receptors to levels of normal function in the CNS perioperatively and several hours post- operatively, yielding neuroprotective effects [5,70]. …”

Section: Mechanismsmentioning

confidence: 99%

Iatrogenic Risk Factors for Alzheimer's Disease: Surgery and Anesthesia

Vanderweyde

Bednar

Forman

et al. 2010

JAD

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Increasing evidence indicates that patients develop post-operative cognitive decline (POCD) following surgery, with risk factors including increasing age, diabetes and low education. POCD is characterized by a bimodal incidence. Initially, there is a transient short-term decline in cognitive ability evident in the early post-operative period. This initial decline predicts a delayed cognitive decline associated with dementia 3 to 5 years post-surgery, with conversion rates up to 70% in patients who are 65 years or older. The factors responsible for this emergence of dementia are unclear and might differ for the acute post-operative emergence of cognitive decline and the subsequent delayed emergence of dementia. Clinical studies investigating the prevalence of POCD and dementia following surgery do not show an association with the type of anesthesia or duration of surgery. However, animal studies suggest that prolonged exposure to some volatile-inhalational anesthetics increase production of Aβ and vulnerability to neurodegeneration. Other factors might include the initiation of an inflammatory response, related to the use of indwelling devices such as the cardio-pulmonary bypass machine or initiated by intrinsic factors such as blood loss, as well as the effects of a maladaptive stress response. Identifying the factors occurring during surgery that predispose subjects to POCD and dementia and subsequent ways to provide prophylaxis against this represent important avenues of research for the health care community. Equally important, the field needs to adopt a more rigorous approach to codifying the frequency and extent of early and delayed post-operative cognitive decline.

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Cerebrospinal fluid concentrations of atracurium, laudanosine and vecuronium following clinical subarachnoid hemorrhage

Abstract: Significant concentrations of atracurium and laudanosine but not of vecuronium were detected in the CSF of patients during and immediately after intracranial aneurysm surgery.

Cited by 26 publications

References 32 publications

Neuronal Effects of Sugammadex in combination with Rocuronium or Vecuronium

Neuronal Effects of Sugammadex in combination with Rocuronium or Vecuronium

In reply

Iatrogenic Risk Factors for Alzheimer's Disease: Surgery and Anesthesia

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