Memory Facilitation by Posttraining Exposure to Halothane, Enflurane, and Isoflurane in ddN Mice

Komatsu, Hisao; Nogaya, Junko; Anabuki, Daisuke; Yokono, Satoshi; Kinoshita, Hiroyuki; Shirakawa, Yoichi; Ogli, Kenji

doi:10.1213/00000539-199303000-00028

Cited by 25 publications

(17 citation statements)

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“…Although patients often regain consciousness quickly after general anesthesia with volatile anesthetics, there is a growing concern of volatile anesthetic safety in recent years. Cognitive impairment in rats can be detected at least 3 weeks after being exposed to volatile anesthetics [7,8], although improvement of cognitive functions after volatile anesthetic exposure in rodents also has been reported [7,9,10]. Volatile anesthetics increase activated caspase 3 expression and β-amyloid peptide (Aβ) production in mouse brains [11].…”

Section: Introductionmentioning

confidence: 99%

Lidocaine attenuates cognitive impairment after isoflurane anesthesia in old rats

Lin

Cao

Wang

et al. 2012

Behavioural Brain Research

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Post-operative cognitive dysfunction (POCD) is a clinical phenomenon that has drawn significant attention from the public and scientific community. Age is a risk factor for POCD. However, the contribution of general anesthesia/anesthetics to POCD and the underlying neuropathology are not clear. Here, we showed that 18-month-old male Fisher 344 rats exposed to 1.2% isoflurane, a general anesthetic, for 2 h had significant learning and memory impairments assessed at 2 to 4 weeks after isoflurane exposure. These isoflurane effects were attenuated by intravenous lidocaine (1.5 mg/kg as a bolus and then 2 mg/kg/h during isoflurane exposure), a local anesthetic that has neuroprotective effect. Exposure to isoflurane or isoflurane plus lidocaine did not change the neuronal and synaptic density as well as the expression of NeuN (a neuronal protein), drebrin (a dendritic spine protein), synaptophysin (a synaptic protein), activated caspase 3 and caspase-activated DNase in the hippocampus at 29 days after isoflurane exposure when cognitive impairment was present. Isoflurane and lidocaine did not affect the amount of β-amyloid peptide, total tau and phospho-tau in the cerebral cortex as well as interleukin-1β and tumor necrosis factor-α in the hippocampus at 29 days after isoflurane exposure. Thus, isoflurane induces learning and memory impairment in old rats. Lidocaine attenuates these isoflurane effects. Isoflurane may not cause long-lasting neuropathological changes.

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Section: Introductionmentioning

confidence: 99%

Lidocaine attenuates cognitive impairment after isoflurane anesthesia in old rats

Lin

Cao

Wang

et al. 2012

Behavioural Brain Research

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“…Such a memory-enhancing effect in young animals had been demonstrated previously with the use of a nonspatial task 22 h after anesthesia administration. 12 A comparative study of rats aged 7 or 60 days showed that 4 h of isoflurane caused a permanent deficit of hippocampal-dependent but not hippocampalindependent learning and memory in 7-day-old rats, whereas 60-day-old animals showed a long-term improvement in spatial reference memory. 13 Concerning the acquisition of new tasks, recent studies have demonstrated learning impairment 24 h and 2 weeks after anesthesia in aged rats, 14 whereas adult rats showed improved learning.…”

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confidence: 99%

Lower Isoflurane Concentration Affects Spatial Learning and Neurodegeneration in Adult Mice Compared with Higher Concentrations

et al. 2010

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Background: Volatile anesthetics such as isoflurane are widely used in clinical and research contexts. Concerns have been raised that the effects of these drugs on the central nervous system may result in long-term impairment after surgery or general anesthesia. Hence, this study aimed to detect how different isoflurane concentrations influence spatial learning and cell death in adult mice. Methods: Fifty-two C57BL/6 mice were randomly divided in four groups. Mice in three groups were exposed to different concentrations of isoflurane (1, 1.5, and 2%) for 1 h; the control group was not exposed to anesthesia. Five mice per group were killed 3 h after anesthesia to perform histopathologic and immunohistochemical analyses (hematoxylin-eosin staining; caspase-3 activation). Eight mice per group were used for behavioral tests (open field, T-maze spontaneous alternation, and water maze) on subsequent days. Results: There were no differences between groups in the T-maze spontaneous alternation test or in the open field (no confounding effects of stress or locomotion). The group anesthetized with 1% isoflurane performed worse in the water maze task on day 1 (550.4 Ϯ162.78 cm) compared with the control group (400.1 Ϯ 112.88 cm), 1.5% isoflurane (351.9 Ϯ 150.67 cm), and 2% isoflurane (364.5 Ϯ 113.70 cm; P Յ 0.05) and on day 3 (305.0 Ϯ 81.75 cm) compared with control group (175.13 Ϯ 77.00 cm) and 2% isoflurane (204.11 Ϯ 85.75 cm; P Յ 0.038). In the pyramidal cell layer of the region cornu ammonis 1 of the hippocampus, 1% isoflurane showed a tendency to cause more neurodegeneration (apoptosis) (61.4 Ϯ 26.40, profiles/mm 2 ) than the group with 2% of isoflurane (20.6 Ϯ 17.77, profiles/mm 2 ; P ϭ 0.051). Conclusion: Low isoflurane concentration (1%) caused spatial learning impairment and more neurodegeneration compared with higher isoflurane concentrations. Results for mice receiving the latter concentrations were similar to those of control mice.

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“…This indings are supported by preclinical studies, which suggest that isolurane anaesthesia administered at clinically relevant doses causes longterm cognitive impairment in unoperated animals [33][34][35]. However, other studies point towards an enhancement of the cognitive functions after anaesthesia inhalation [36][37][38].…”

Section: Introductionmentioning

confidence: 79%

Postoperative Cognitive Dysfunction: Preclinical Highlights and Perspectives on Preventive Strategies

Locatelli¹,

Kawano²

2017

Current Topics in Anesthesiology

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One of the common complications associated with anaesthesia and surgery in geriatric patients is the postoperative cognitive dysfunction (POCD). This cognitive impairment afects the long-term prognosis and has been shown to be associated with long-term disability, higher health care costs, and even increased mortality. On the other hand, clinical research on POCD is in its infancy, the condition has not been clariied, and since no strategy for management is currently available, it is imperative to develop speciic methods for prevention and management. Although its pathogenesis involves various factors, accumulating evidence suggests that surgery elicits an inlammatory response in the hippocampus, a brain area closely related to cognitive function, playing a key role in the development of POCD. Several studies suggest that age-related phenotypic change of microglia is associated with pathogenic neuroinlammation, and more importantly it may be modiiable. In this chapter, we discuss the current overview and preclinical highlights regarding POCD. We further discuss some perspectives on preventive strategies for POCD, based on the indings of our preclinical research and the available literature.

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Memory Facilitation by Posttraining Exposure to Halothane, Enflurane, and Isoflurane in ddN Mice

Cited by 25 publications

References 0 publications

Lidocaine attenuates cognitive impairment after isoflurane anesthesia in old rats

Lidocaine attenuates cognitive impairment after isoflurane anesthesia in old rats

Lower Isoflurane Concentration Affects Spatial Learning and Neurodegeneration in Adult Mice Compared with Higher Concentrations

Postoperative Cognitive Dysfunction: Preclinical Highlights and Perspectives on Preventive Strategies

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