The Healing Powers of Anesthetics

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The Healing Powers of Anesthetics

Postby sixwings » Wed Aug 07, 2013 6:02 pm

Anesthetics have amazing therapeutic powers that go beyond simple anesthesia. This thread is reserved for articles, news, links and studies about the healing powers of anesthetics.
Louis Savain
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Re: The Healing Powers of Anesthetics

Postby sixwings » Wed Aug 07, 2013 6:05 pm

Shocking: Surgical Anesthetic Appears to Treat Drug-Resistant Depression
In a pilot study with 20 patients who received ECT treatments compared to eight patients who received the isoflurane treatments, the researchers found that both therapies provided significant reduction in symptoms of depression. Immediately following the treatments, ECT patients showed declines in areas of memory, verbal fluency, and processing speed. Most of these ECT-related deficits did resolve by four weeks. However, autobiographical memory, or recall of personal life events, remained below pretreatment levels for ECT patients four weeks after the treatment. In contrast, the patients treated with isoflurane showed no real impairment but instead had greater improvements in cognitive testing than ECT patients both immediately and 4 weeks after the treatments.

Read the full article.
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Re: The Healing Powers of Anesthetics

Postby sixwings » Thu Aug 08, 2013 10:05 am

This study shows the power of anesthetics to affect neurodegenerative diseases like multiple sclerosis. Emphasis added.

Sevoflurane reduces clinical disease in a mouse model of multiple sclerosis

Paul E Polak, Randall O Dull, Sergey Kalinin, Anthony J Sharp, Richard Ripper, Guy Weinberg, David E Schwartz, Israel Rubinstein and Douglas L Feinstein

Corresponding author: Douglas L Feinstein dlfeins@uic.edu

Abstract

Background

Inhalational anesthetics have been shown to influence T cell functions both in vitro and in vivo, in many cases inducing T cell death, suggesting that exposure to these drugs could modify the course of an autoimmune disease. We tested the hypothesis that in mice immunized to develop experimental autoimmune encephalomyelitis (EAE), a well established model of multiple sclerosis (MS), treatment with the commonly used inhalational anesthetic sevoflurane would attenuate disease symptoms.

Methods

C57Bl6 female mice were immunized with myelin oligodendrocyte glycoprotein (MOG) peptide residues 35 to 55 to induce a chronic demyelinating disease. At day 10 after immunization, the mice were subjected to 2 h of 2.5% sevoflurane in 100% oxygen, or 100% oxygen, alone. Following treatment, clinical scores were monitored up to 4 weeks, after which brain histology was performed to measure the effects on astrocyte activation and lymphocyte infiltration. Effects of sevoflurane on T cell activation were studied using splenic T cells isolated from MOG peptide-immunized mice, restimulated ex vivo with MOG peptide or with antibodies to CD3 and CD28, and in the presence of different concentrations of sevoflurane. T cell responses were assessed 1 day later by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay for proliferation, lactate dehydrogenase (LDH) release for cell death, and inflammatory activation by production of interleukin (IL)-17 and interferon (IFN)γ.

Results

Clinical scores in the oxygen-treated group increased until day 28 at which time they showed moderate to severe disease (average clinical score of 2.9). In contrast, disease progression in the sevoflurane-treated group increased to 2.1 at day 25, after which it remained unchanged until the end of the study. Immunohistochemical analysis revealed reduced numbers of infiltrating leukocytes and CD4+ cells in the CNS of the sevoflurane-treated mice, as well as reduced glial cell activation. In splenic T cells, low doses of sevoflurane reduced IFNγ production, cell proliferation, and increased LDH release.

Conclusions

These results are the first to show attenuation of EAE disease by an inhaled anesthetic and are consistent with previous reports that inhaled anesthetics, including sevoflurane, can suppress T cell activation that, in the context of autoimmune diseases such as MS, could lead to reduced clinical progression.

Source: http://www.jneuroinflammation.com/content/9/1/272
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