An assessment of the cerebroprotective potential of volatile anaesthetics using two independent methods in an in vitro model of cerebral ischaemia

Toner, Christopher C.; Milne, Andrew; Blatchford, Karen L; McLaughlin, Daniel P.; Stamford, Jonathan A.

doi:10.1016/s0006-8993(02)03696-x

Cited by 14 publications

(12 citation statements)

References 24 publications

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“…However, halothane in rat mixed neuronastrocyte cultures failed to protect against oxidative stress induced by hydrogen peroxide or xanthinexanthine oxidase yet was protective against ironinduced cytotoxicity (Kudo et al, 2001a). Furthermore, toxic effects were observed in rat corticostriatal brain slices treated with halothane and OGD (Toner et al, 2002). As with isoflurane, halothane is more likely to be neuroprotective at lower doses and Abbreviations: CAO, carotid artery occlusion; EEG, electroencephalogram; MCAO, middle cerebral artery occlusion; MAC, minimal alveolar concentration.…”

Section: Halothanementioning

confidence: 99%

“…Post-MCAO treatment with xenon has also been reported to reduce cortical brain damage (Abraini et al, 2005;David et al, 2003). Another agent, enflurane, has been observed to have limited striatal protective effects in vitro (Toner et al, 2002). However, no animal studies have been performed evaluating enflurane's neuroprotective potential during cerebral ischemia.…”

Section: Other Volatile Anestheticsmentioning

confidence: 99%

“…k or no effect Not determined Koorn et al (1993); Toner et al (2002) k k or no effect Engelhard et al (1999), Mackensen et al (1999), Halothane No effect Not determined Koorn et al (1993); Toner et al (2002) Sevoflurane k or inconsistent effect…”

Section: Isofluranementioning

confidence: 99%

See 2 more Smart Citations

Inhalational Anesthetics as Neuroprotectants or Chemical Preconditioning Agents in Ischemic Brain

Kitano

Kirsch

Hurn

et al. 2006

J Cereb Blood Flow Metab

179

128

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This review will focus on inhalational anesthetic neuroprotection during cerebral ischemia and inhalational anesthetic preconditioning before ischemic brain injury. The limitations and challenges of past and current research in this area will be addressed before reviewing experimental and clinical studies evaluating the effects of inhalational anesthetics before and during cerebral ischemia. Mechanisms underlying volatile anesthetic neuroprotection and preconditioning will also be examined. Lastly, future directions for inhalational anesthetics and ischemic brain injury will be briefly discussed.

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Section: Halothanementioning

confidence: 99%

Section: Other Volatile Anestheticsmentioning

confidence: 99%

See 1 more Smart Citation

Inhalational Anesthetics as Neuroprotectants or Chemical Preconditioning Agents in Ischemic Brain

Kitano

Kirsch

Hurn

et al. 2006

J Cereb Blood Flow Metab

179

128

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“…In healthy tissues, TTC is converted to a red, insoluble formazan (1,3,5-triphenylformazan) by complex II of oxidative phosphorylation in mitochondria. Thus, cells which are dead or which have impaired oxidative metabolism do not stain or stain less than healthy cells [33].…”

Section: Histochemical Analysesmentioning

confidence: 99%

Age-dependent MRI-detected lesions at early stages of transient global ischemia in rat brain

Canese

Lorenzini

Fortuna

et al. 2004

MAGMA

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Although ischemic stroke has higher incidence and severity in aged than in young humans, the age factor is generally neglected in ischemia animal models. This study was aimed at comparing age-dependent effects at early stages of transient global cerebral ischemia (TGCI) in rats. TGCI was induced in two groups of rats (3-6 and 20-24 months old, respectively) by exposure to 15% oxygen and 15 min occlusion of the two common carotid arteries. Brains were analysed in vivo by MRI-apparent diffusion coefficient (ADC) and T2 maps--at 1-3 h post-TGCI and in vitro by histochemical examination of triphenyltetrazolium chloride (TTC)-stained slices. At 1-3 h post-TGCI, a higher incidence of lesions was found in aged than in young rats especially in the hippocampus and cortex (occipital plus parietal) but not in the thalamus. The lesioned regions showed lower ADC values in aged than in younger rats. The most substantial ADC decreases were associated with enhanced spin-spin relaxation and lower TTC staining. The different responses of the two age groups support the use of aged animals for investigations on different ischemia models. Our model of brain ischemia appears appropriate for further studies including drug effects.

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“…After post‐OGD incubation, slices were stained with TTC (2% w/v in 0.9% NaCl) at room temperature in the dark for 30 min, fixed in 4% paraformaldehyde solution and stored overnight at 4 °C. Stained slices were photographed, together with a calibration scale (1‐mm divisions), and analysed for the percentage of striatal area stained or unstained (29) using scion image software (Version Beta 4.0.2; Scion Corporation, Frederick, MD, USA).…”

Section: Methodsmentioning

confidence: 99%

Allopregnanolone Protects Against Dopamine‐Induced Striatal Damage After In Vitro Ischaemia via Interaction at GABA_A Receptors

Knight

Davidson

Young

et al. 2012

J Neuroendocrinology

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Sex steroid hormones, such as progesterone, have been shown to display neuroprotective properties after various models of central nervous system injury, including cerebral ischaemia, although the mechanism(s) of action remain largely undetermined. Allopregnanolone, an active progesterone metabolite, may explain some of the protective actions of progesterone. We utilised an in vitro model of ischaemia to evaluate the neuroprotective potential of allopregnanolone and examine its interaction at the GABA(A) receptor, which is hypothesised to be its main neuroprotective mechanism. In adult male mouse coronal caudate slices exposed to oxygen glucose deprivation (OGD), we measured aspects of OGD-induced dopamine release, which is neurotoxic during ischaemia, using fast cyclic voltammetry and also assessed tissue viability. The GABA(A) agonist, muscimol, displayed a neuroprotective profile in terms of delaying the OGD-evoked dopamine efflux (P< 0.05) and reducing the amount of dopamine released after OGD (P < 0.05). Allopregnanolone, at a concentration of 10(-6) m, also displayed a neuroprotective profile because it significantly reduced the amount of dopamine efflux (P < 0.05) and reduced the loss of viable tissue after OGD compared to slices exposed to vehicle during OGD (P < 0.05). However, the effect of 10(-6) m allopregnanolone on dopamine efflux was prevented in the presence of bicuculline, a competitive GABA(A) receptor antagonist. These results describe the use of an in vitro model of ischaemia with respect to determining that allopregnanolone is neuroprotective during the acute phase of ischaemia, and also demonstrate that such actions are dependent, at least in part, upon interaction at the GABA(A) receptor.

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An assessment of the cerebroprotective potential of volatile anaesthetics using two independent methods in an in vitro model of cerebral ischaemia

Cited by 14 publications

References 24 publications

Inhalational Anesthetics as Neuroprotectants or Chemical Preconditioning Agents in Ischemic Brain

Inhalational Anesthetics as Neuroprotectants or Chemical Preconditioning Agents in Ischemic Brain

Age-dependent MRI-detected lesions at early stages of transient global ischemia in rat brain

Allopregnanolone Protects Against Dopamine‐Induced Striatal Damage After In Vitro Ischaemia via Interaction at GABA_A Receptors

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An assessment of the cerebroprotective potential of volatile anaesthetics using two independent methods in an in vitro model of cerebral ischaemia

Cited by 14 publications

References 24 publications

Inhalational Anesthetics as Neuroprotectants or Chemical Preconditioning Agents in Ischemic Brain

Inhalational Anesthetics as Neuroprotectants or Chemical Preconditioning Agents in Ischemic Brain

Age-dependent MRI-detected lesions at early stages of transient global ischemia in rat brain

Allopregnanolone Protects Against Dopamine‐Induced Striatal Damage After In Vitro Ischaemia via Interaction at GABAA Receptors

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Product

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Allopregnanolone Protects Against Dopamine‐Induced Striatal Damage After In Vitro Ischaemia via Interaction at GABA_A Receptors