Assessment of Postischemic Neurogenesis in Rats with Cerebral Ischemia and Propofol Anesthesia

Lasarzik, Irina; Winkelheide, Uta; Stallmann, Sonja; Orth, C; Schneider, Astrid; Tresch, Achim; Werner, Christian; Engelhard, Kristin

doi:10.1097/aln.0b013e318195b4fe

Cited by 23 publications

(13 citation statements)

References 36 publications

(32 reference statements)

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“…34 Finally, the preclinical data do not support a difference between propofol and the halogenated agents in terms of putative prevention of neuropathy, as both may act on the peripheral fibres 35,36 and may even have some neuroprotective effects. 37,38 Although it might be possible to explain the discrepancy between our results and those of Cho et al 10 by examining the mechanisms, it may also be explained by different methodologies. Our design had a greater sample size, standardised times of measurement of PPSP and a multicentre setting.…”

Section: Discussioncontrasting

confidence: 69%

General anaesthetic agents do not influence persistent pain after breast cancer surgery

Lefebvre-Kuntz

Dualé

Albi-Feldzer

et al. 2015

European Journal of Anaesthesiology

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Section: Discussioncontrasting

confidence: 69%

General anaesthetic agents do not influence persistent pain after breast cancer surgery

Lefebvre-Kuntz

Dualé

Albi-Feldzer

et al. 2015

European Journal of Anaesthesiology

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“…46,47 Such controversy may be due to confounding variables in the use of animal models. 48,49 In an attempt to reduce such variables, we chose to study neural progenitor cells in vitro. Our results suggested that at clinically relevant concentrations of propofol, proliferation contributed more to the increased cell viability than differentiation.…”

Section: Discussionmentioning

confidence: 99%

Propofol Affects Neurodegeneration and Neurogenesis by Regulation of Autophagy via Effects on Intracellular Calcium Homeostasis

Qiao

et al. 2017

Anesthesiology

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Background In human cortical neural progenitor cells, we investigated the effects of propofol on calcium homeostasis in both the ryanodine and inositol 1,4,5-trisphosphate calcium release channels. We also studied propofol-mediated effects on autophagy, cell survival, and neuro- and gliogenesis. Methods The dose–response relationship between propofol concentration and duration was studied in neural progenitor cells. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase release assays. The effects of propofol on cytosolic calcium concentration were evaluated using Fura-2, and autophagy activity was determined by LC3II expression levels with Western blot. Proliferation and differentiation were evaluated by bromodeoxyuridine incorporation and immunostaining with neuronal and glial markers. Results Propofol dose- and time-dependently induced cell damage and elevated LC3II expression, most robustly at 200 µM for 24 h (67 ± 11% of control, n = 12 to 19) and 6 h (2.4 ± 0.5 compared with 0.6 ± 0.1 of control, n = 7), respectively. Treatment with 200 μM propofol also increased cytosolic calcium concentration (346 ± 71% of control, n = 22 to 34). Propofol at 10 µM stimulated neural progenitor cell proliferation and promoted neuronal cell fate, whereas propofol at 200 µM impaired neuronal proliferation and promoted glial cell fate (n = 12 to 20). Cotreatment with ryanodine and inositol 1,4,5-trisphosphate receptor antagonists and inhibitors, cytosolic Ca2+ chelators, or autophagy inhibitors mostly mitigated the propofol-mediated effects on survival, proliferation, and differentiation. Conclusions These results suggest that propofol-mediated cell survival or neurogenesis is closely associated with propofol’s effects on autophagy by activation of ryanodine and inositol 1,4,5-trisphosphate receptors.

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“…Propofol has been reported to be beneficial in focal [109, 110], hemispheric [111], and global [112-114] ischemic insults. These positive results have been countered by other work, which failed to detect an effect on outcome in vivo [115-117] or in vitro [53]. α-2-agonists are a class of compounds including dexmedetomidine, clonidine, and xylazine.…”

Section: Ischemic Outcomementioning

confidence: 97%

Anesthesia in Experimental Stroke Research

Hoffmann

Sheng

Ayata

et al. 2016

Transl. Stroke Res.

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Anesthetics have enabled major advances in development of experimental models of human stroke. Yet their profound pharmacologic effects on neural function can confound the interpretation of experimental stroke research. Anesthetics have drug and dose-specific effects on cerebral blood flow and metabolism, neurovascular coupling, autoregulation, ischemic depolarizations, excitotoxicity, inflammation, neural networks, and numerous molecular pathways relevant for stroke outcome. Both pre- and post-conditioning properties have been described. Anesthetics also modulate systemic arterial blood pressure, lung ventilation, and thermoregulation, all of which may interact with the ischemic insult as well as the therapeutic interventions. These confounds present a dilemma. Here, we provide an overview of the anesthetic mechanisms of action and molecular and physiologic effects on factors relevant to stroke outcomes that can guide the choice and optimization of the anesthetic regimen in experimental stroke.

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Assessment of Postischemic Neurogenesis in Rats with Cerebral Ischemia and Propofol Anesthesia

Cited by 23 publications

References 36 publications

General anaesthetic agents do not influence persistent pain after breast cancer surgery

General anaesthetic agents do not influence persistent pain after breast cancer surgery

Propofol Affects Neurodegeneration and Neurogenesis by Regulation of Autophagy via Effects on Intracellular Calcium Homeostasis

Anesthesia in Experimental Stroke Research

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