Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice
In rodents, neonatal sevoflurane exposure induces neonatal apoptosis in the brain and results in learning deficits. Sugammadex is a new selective neuromuscular blockade (NMB) binding agent that anesthesiologists can use to achieve immediate reversal of an NMB with few side effects. Given its molecul...
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| Format: | Article |
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Wiley
2016-01-01
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| Series: | Anesthesiology Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2016/9682703 |
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| author | Maiko Satomoto Zhongliang Sun Yushi U. Adachi Koshi Makita |
| author_facet | Maiko Satomoto Zhongliang Sun Yushi U. Adachi Koshi Makita |
| author_sort | Maiko Satomoto |
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| description | In rodents, neonatal sevoflurane exposure induces neonatal apoptosis in the brain and results in learning deficits. Sugammadex is a new selective neuromuscular blockade (NMB) binding agent that anesthesiologists can use to achieve immediate reversal of an NMB with few side effects. Given its molecular weight of 2178, sugammadex is thought to be unable to pass through the blood brain barrier (BBB). Volatile anesthetics can influence BBB opening and integrity. Therefore, we investigated whether the intraperitoneal administration of sugammadex could exacerbate neuronal damage following neonatal 2% sevoflurane exposure via changes in BBB integrity. Cleaved caspase-3 immunoblotting was used to detect apoptosis, and the ultrastructure of the BBB was examined by transmission electron microscopy. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice. Sugammadex alone without sevoflurane did not induce apoptosis. The coadministration of sugammadex with sevoflurane to neonatal mice caused a significant increase (150%) in neuroapoptosis in the brain compared with 2% sevoflurane. In neonatal anesthesia, sugammadex could influence neurotoxicity together with sevoflurane. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice. |
| format | Article |
| id | doaj-art-b1e01f4ff82b4714babe5807c554b688 |
| institution | Kabale University |
| issn | 1687-6962 1687-6970 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
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| series | Anesthesiology Research and Practice |
| spelling | doaj-art-b1e01f4ff82b4714babe5807c554b6882025-02-03T01:32:13ZengWileyAnesthesiology Research and Practice1687-69621687-69702016-01-01201610.1155/2016/96827039682703Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in MiceMaiko Satomoto0Zhongliang Sun1Yushi U. Adachi2Koshi Makita3Department of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 1138519, JapanDepartment of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 1138519, JapanDepartment of Anesthesiology, Graduate School of Medicine, Nagoya University, Aichi, JapanDepartment of Anesthesiology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 1138519, JapanIn rodents, neonatal sevoflurane exposure induces neonatal apoptosis in the brain and results in learning deficits. Sugammadex is a new selective neuromuscular blockade (NMB) binding agent that anesthesiologists can use to achieve immediate reversal of an NMB with few side effects. Given its molecular weight of 2178, sugammadex is thought to be unable to pass through the blood brain barrier (BBB). Volatile anesthetics can influence BBB opening and integrity. Therefore, we investigated whether the intraperitoneal administration of sugammadex could exacerbate neuronal damage following neonatal 2% sevoflurane exposure via changes in BBB integrity. Cleaved caspase-3 immunoblotting was used to detect apoptosis, and the ultrastructure of the BBB was examined by transmission electron microscopy. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice. Sugammadex alone without sevoflurane did not induce apoptosis. The coadministration of sugammadex with sevoflurane to neonatal mice caused a significant increase (150%) in neuroapoptosis in the brain compared with 2% sevoflurane. In neonatal anesthesia, sugammadex could influence neurotoxicity together with sevoflurane. Exposure to 2% sevoflurane for 6 h resulted in BBB ultrastructural abnormalities in the hippocampus of neonatal mice.http://dx.doi.org/10.1155/2016/9682703 |
| spellingShingle | Maiko Satomoto Zhongliang Sun Yushi U. Adachi Koshi Makita Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice Anesthesiology Research and Practice |
| title | Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice |
| title_full | Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice |
| title_fullStr | Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice |
| title_full_unstemmed | Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice |
| title_short | Sugammadex-Enhanced Neuronal Apoptosis following Neonatal Sevoflurane Exposure in Mice |
| title_sort | sugammadex enhanced neuronal apoptosis following neonatal sevoflurane exposure in mice |
| url | http://dx.doi.org/10.1155/2016/9682703 |
| work_keys_str_mv | AT maikosatomoto sugammadexenhancedneuronalapoptosisfollowingneonatalsevofluraneexposureinmice AT zhongliangsun sugammadexenhancedneuronalapoptosisfollowingneonatalsevofluraneexposureinmice AT yushiuadachi sugammadexenhancedneuronalapoptosisfollowingneonatalsevofluraneexposureinmice AT koshimakita sugammadexenhancedneuronalapoptosisfollowingneonatalsevofluraneexposureinmice |