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Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury
BACKGROUND: Dexmedetomidine is a highly selective adrenergic receptor agonist, which has a dose-dependent sedative hypnotic effect. Furthermore, it also has pharmacological properties, and the ability to inhibit sympathetic activity and improve cardiovascular stability during an operation. However,...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5607498/ https://www.ncbi.nlm.nih.gov/pubmed/28931374 http://dx.doi.org/10.1186/s12871-017-0410-7 |
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author | Jiang, Wan-Wei Wang, Qing-Hui Liao, Ya-Jing Peng, Pai Xu, Min Yin, Li-Xin |
author_facet | Jiang, Wan-Wei Wang, Qing-Hui Liao, Ya-Jing Peng, Pai Xu, Min Yin, Li-Xin |
author_sort | Jiang, Wan-Wei |
collection | PubMed |
description | BACKGROUND: Dexmedetomidine is a highly selective adrenergic receptor agonist, which has a dose-dependent sedative hypnotic effect. Furthermore, it also has pharmacological properties, and the ability to inhibit sympathetic activity and improve cardiovascular stability during an operation. However, its protective effect on patients with severe craniocerebral injury in the perioperative period remains unclear. METHOD: Eighty adult male SD rats were used and divided into two groups (n = 40, each group): dexmedetomidine injury group (experimental group), and sodium chloride injury group (control group). Models of severe craniocerebral injury were established in these two groups using the modified Feeney’s free-fall method. As soon as the establishment of models was succeed, rat in the experimental group received 1 μg of dexmedetomidine (0.1 ml), while each rat in the control group was given 0.1 ml of 0.9% sodium chloride. Blood was sampled from an incision at the femoral vein to detect TNF-α and IL-2 levels at 1, 12, 24,36,48 and 72 h after establishing the model in the two groups. RESULTS: After severe craniocerebral injury, TNF-α levels of rats were lower in every stage and at different degrees in the experimental group than in the control group (P < 0.05), while IL-2 levels were lower in the experimental group to different extents (P < 0.05). CONCLUSION: Dexmedetomidine protects the brain of rats with severe craniocerebral injury by reducing the release of inflammatory mediators. |
format | Online Article Text |
id | pubmed-5607498 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-56074982017-09-24 Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury Jiang, Wan-Wei Wang, Qing-Hui Liao, Ya-Jing Peng, Pai Xu, Min Yin, Li-Xin BMC Anesthesiol Research Article BACKGROUND: Dexmedetomidine is a highly selective adrenergic receptor agonist, which has a dose-dependent sedative hypnotic effect. Furthermore, it also has pharmacological properties, and the ability to inhibit sympathetic activity and improve cardiovascular stability during an operation. However, its protective effect on patients with severe craniocerebral injury in the perioperative period remains unclear. METHOD: Eighty adult male SD rats were used and divided into two groups (n = 40, each group): dexmedetomidine injury group (experimental group), and sodium chloride injury group (control group). Models of severe craniocerebral injury were established in these two groups using the modified Feeney’s free-fall method. As soon as the establishment of models was succeed, rat in the experimental group received 1 μg of dexmedetomidine (0.1 ml), while each rat in the control group was given 0.1 ml of 0.9% sodium chloride. Blood was sampled from an incision at the femoral vein to detect TNF-α and IL-2 levels at 1, 12, 24,36,48 and 72 h after establishing the model in the two groups. RESULTS: After severe craniocerebral injury, TNF-α levels of rats were lower in every stage and at different degrees in the experimental group than in the control group (P < 0.05), while IL-2 levels were lower in the experimental group to different extents (P < 0.05). CONCLUSION: Dexmedetomidine protects the brain of rats with severe craniocerebral injury by reducing the release of inflammatory mediators. BioMed Central 2017-09-20 /pmc/articles/PMC5607498/ /pubmed/28931374 http://dx.doi.org/10.1186/s12871-017-0410-7 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Jiang, Wan-Wei Wang, Qing-Hui Liao, Ya-Jing Peng, Pai Xu, Min Yin, Li-Xin Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury |
title | Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury |
title_full | Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury |
title_fullStr | Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury |
title_full_unstemmed | Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury |
title_short | Effects of dexmedetomidine on TNF-α and interleukin-2 in serum of rats with severe craniocerebral injury |
title_sort | effects of dexmedetomidine on tnf-α and interleukin-2 in serum of rats with severe craniocerebral injury |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5607498/ https://www.ncbi.nlm.nih.gov/pubmed/28931374 http://dx.doi.org/10.1186/s12871-017-0410-7 |
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