Anesthetic drugs and sustained neuroprotection in acute cerebral ischemia: can we alter clinical outcomes?

Werner, Christian

doi:10.1007/s12630-009-9166-y

Cited by 3 publications

(3 citation statements)

References 24 publications

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“…The extent of increase differed depending on the anesthetics - being highest with isoflurane and lowest with sevoflurane. Apart from neuroprotective effects of volatile anesthetics [27], [28], different anesthetics also increase cerebral water content in animals with or without brain injury [7]. Currently no data is available on the effect of sevoflurane on BBB integrity and brain edema formation during TBI.…”

Section: Discussionmentioning

confidence: 99%

Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury

et al. 2012

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Disruption of the blood-brain barrier (BBB) results in cerebral edema formation, which is a major cause for high mortality after traumatic brain injury (TBI). As anesthetic care is mandatory in patients suffering from severe TBI it may be important to elucidate the effect of different anesthetics on cerebral edema formation. Tight junction proteins (TJ) such as zonula occludens-1 (ZO-1) and claudin-5 (cl5) play a central role for BBB stability. First, the influence of the volatile anesthetics sevoflurane and isoflurane on in-vitro BBB integrity was investigated by quantification of the electrical resistance (TEER) in murine brain endothelial monolayers and neurovascular co-cultures of the BBB. Secondly brain edema and TJ expression of ZO-1 and cl5 were measured in-vivo after exposure towards volatile anesthetics in native mice and after controlled cortical impact (CCI). In in-vitro endothelial monocultures, both anesthetics significantly reduced TEER within 24 hours after exposure. In BBB co-cultures mimicking the neurovascular unit (NVU) volatile anesthetics had no impact on TEER. In healthy mice, anesthesia did not influence brain water content and TJ expression, while 24 hours after CCI brain water content increased significantly stronger with isoflurane compared to sevoflurane. In line with the brain edema data, ZO-1 expression was significantly higher in sevoflurane compared to isoflurane exposed CCI animals. Immunohistochemical analyses revealed disruption of ZO-1 at the cerebrovascular level, while cl5 was less affected in the pericontusional area. The study demonstrates that anesthetics influence brain edema formation after experimental TBI. This effect may be attributed to modulation of BBB permeability by differential TJ protein expression. Therefore, selection of anesthetics may influence the barrier function and introduce a strong bias in experimental research on pathophysiology of BBB dysfunction. Future research is required to investigate adverse or beneficial effects of volatile anesthetics on patients at risk for cerebral edema.

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Section: Discussionmentioning

confidence: 99%

Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury

et al. 2012

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“…In aggregate, the clinical evidence is less convincing, although experimental data support the neuroprotective effects of volatile anesthetics. The clinical results may be explained by the view that a single pharmacological approach can hardly affect the multiple simultaneous pathological events in patients with the parallel variability of coexisting disease (104). Furthermore, most studies have utilized indirect markers, such as critical rCBF and S100-beta protein, for clinical assessment of volatile anesthetic neuroprotection.…”

Section: Clinical Studiesmentioning

confidence: 99%

Neuroprotections and mechanisms of inhalational anesthetics against brain ischemia

Wang²,

Gao³

et al. 2010

Front Biosci

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The new generation of inhalational anesthetics has been widely used for general anesthesia in both clinical and experimental settings because of their safety, reliability and potency. A neuroprotective role has recently been revealed for some of these anesthetics, including the volatile gases isoflurane, sevoflurane, and desflurane, as well as the inert gas xenon. In vivo and in vitro studies have demonstrated that these gases were able to protect brain against ischemic injury, indicated by the decreases in infarct volumes and neuronal apoptosis. In this review, we [Please see table 1] will briefly introduce the properties of these gases, and discuss in detail their effects on brain ischemia, effective treatment regimens, and neuroprotective mechanisms. Perspectives are also discussed on future study and use of inhalational anesthetics.

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“…Xenon (Xe), a noble gas having antiproteolytic properties 12 , is a well-known neuroprotectant in treatment of brain injury 13 – 17 . Unlike other therapeutics, Xe is a small molecule that can rapidly diffuse across the blood-brain barrier (BBB) and transit across cell membranes with no proven adverse side effects 18 , 19 .…”

Section: Introductionmentioning

confidence: 99%

Delivery of xenon-containing echogenic liposomes inhibits early brain injury following subarachnoid hemorrhage

Miao

Peng

Moody

et al. 2018

Sci Rep

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Xenon (Xe), a noble gas, has promising neuroprotective properties with no proven adverse side-effects. We evaluated neuroprotective effects of Xe delivered by Xe-containing echogenic liposomes (Xe-ELIP) via ultrasound-controlled cerebral drug release on early brain injury following subarachnoid hemorrhage (SAH). The Xe-ELIP structure was evaluated by ultrasound imaging, electron microscopy and gas chromatography-mass spectroscopy. Animals were randomly divided into five groups: Sham, SAH, SAH treated with Xe-ELIP, empty ELIP, or Xe-saturated saline. Treatments were administrated intravenously in combination with ultrasound application over the common carotid artery to trigger Xe release from circulating Xe-ELIP. Hematoma development was graded by SAH scaling and quantitated by a colorimetric method. Neurological evaluation and motor behavioral tests were conducted for three days following SAH injury. Ultrasound imaging and electron microscopy demonstrated that Xe-ELIP have a unique two-compartment structure, which allows a two-stage Xe release profile. Xe-ELIP treatment effectively reduced bleeding, improved general neurological function, and alleviated motor function damage in association with reduced apoptotic neuronal death and decreased mortality. Xe-ELIP alleviated early SAH brain injury by inhibiting neuronal death and bleeding. This novel approach provides a noninvasive strategy of therapeutic gas delivery for SAH treatment.

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Anesthetic drugs and sustained neuroprotection in acute cerebral ischemia: can we alter clinical outcomes?

Cited by 3 publications

References 24 publications

Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury

Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury

Neuroprotections and mechanisms of inhalational anesthetics against brain ischemia

Delivery of xenon-containing echogenic liposomes inhibits early brain injury following subarachnoid hemorrhage

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