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BioMed Research International
Volume 2015 (2015), Article ID 575474, 6 pages
Research Article

Prophylactic Antiarrhythmic Effect of Anesthetics at Subanesthetic Concentration on Epinephrine-Induced Arrhythmias in Rats after Brain Death

1Department of Anesthesiology, Osaka University Faculty of Medicine, Suita, Osaka 565-0871, Japan
2Department of Anesthesiology, Sakurabashi-Watanabe Hospital, 2-4-32 Umeda, Kita-ku, Osaka 530-0001, Japan

Received 7 June 2014; Accepted 17 September 2014

Academic Editor: Hideo Inaba

Copyright © 2015 Yuka Miyata et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The present study using brain death model of rats was designed to examine whether prophylactic administration of volatile anesthetics and propofol prevent the epinephrine-induced arrhythmias. A Fogarty catheter was placed intracranially for induction of brain death. After brain death, the rats were randomly assigned to five groups: the control group (no anesthetics), the sevoflurane group (0.8%), the isoflurane group (0.5%), the halothane group (0.3%), and the propofol group (195 μg·kg−1·min−1). These anesthetics were about 30% of of each anesthetic. The arrhythmogenic dose of epinephrine was determined in each anesthetic group. In addition, we examined left ventricular levels of connexin 43 phosphorylation 30 min after administration of each anesthetic with Western blot analysis. The arrhythmogenic dose of epinephrine in the sevoflurane group was significantly higher than that in the control group, while the arrhythmogenic dose of epinephrine in any other anesthetic group was not different. On the other hand, the ratio of phosphorylated-connexin 43/total connexin 43 was also similar among the study groups. Thus, prophylactic administration of subanesthetic dose of sevoflurane is effective in preventing epinephrine-induced arrhythmias after brain death, but phosphorylation of connexin is not involved in the antiarrhythmic property of sevoflurane.