Establishment of a rat model of myocardial mitochondrial damage induced by bupivacaine
Received:July 25, 2018  
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DOI:10. 3969 / j.issn.1005-4847. 2019. 01. 003
KeyWord:electrical stimulation; bupivacaine; cardiomyocyte model; mitochondrial damage; reactive oxygen species
张颖颖 河北北方学院附属第一医院麻醉科,河北张家口 
段然 河北省人民医院麻醉科,石家庄 
陈永学 邯郸市中心医院麻醉科,河北邯郸 
赵森明 河北医科大学第三医院,石家庄 
夏登云 河北北方学院附属第一医院麻醉科,河北张家口 
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      Objective To observe the morphological changes of cardiomyocytic mitochondria and the reactive oxygen species content in bupivacaine-exposed myocardial cells under electrical stimulation, and to establish an ideal myocardial cell model of bupivacaine poisoning. Methods A Langendorff device was used to separate the cardiomyocytes of male SD rats. The cells were divided into four groups randomly: a DMEM static group, DMEM electric stimulation group, bupivacaine static group and bupivacaine plus electric stimulation group. The experiment was repeated for five times.The cardiomyocytic mitochondrial morphology was observed by transmission electron microscopy, and the ROS content was measured with a multifunctional microplate detector. Results The degree of mitochondrial swelling and the ROS content in the DMEM electric stimulation group were not significantly different from those of the DMEM group ( P > 0. 05), but the mitochondrial swelling in the bupivacaine plus electric stimulation group was significantly higher than that of the bupivacaine group ( P =0. 000), and the ROS output was also significantly increased ( P < 0. 05). Conclusions Under electrical stimulation, cardiomyocytes show rhythmic contractions, allowing better simulation of the myocardial mitochondrial injury during clinical bupivacaine poisoning.
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