Establishment of a rat model of bupivacaine-induced cardiomyocyte mitochondrial damage

  OBJECTIVE: To observe the changes in mitochondrial morphology and reactive oxygen species (ROS) production of bupivacaine cardiomyocytes under electrical stimulation, and to explore the establishment of an ideal rat cardiomyocyte model of bupivacaine poisoning. Methods: The Langendroff device was used to freshly isolate the cardiomyocytes of male SD rats. After counting the cells, they were transferred to the doff tube and randomly divided into four groups: DMEM static group, DMEM electrical stimulation group, bupivacaine static group, and bubica Caine electrical stimulation group. The experiment was repeated five times. Transmission electron microscopy was used to observe the morphology of myocardial cell mitochondria, and a multi-functional microplate detector was used to measure the amount of ROS generation. Results: The degree of mitochondrial swelling and ROS generation in the DMEM electrical stimulation group was not significantly different from that of the DMEM static group (P>0.05); while the bupivacaine electrical stimulation group was significantly higher than the bupivacaine static group. Group (P=0.000), and the amount of ROS generation was also significantly increased (P<0.05).

   Conclusion: Myocardial cells contracted rhythmically under electrical stimulation, which can better simulate myocardial mitochondrial damage during clinical bupivacaine poisoning.