【Animal Modeling】-Bupivacaine-induced Myocardial Cell Mitochondria Damage Rat Model

  OBJECTIVE: To observe the changes in mitochondria of bupivacaine cardiomyocytes and the production of reactive oxygen species 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 the cell count, they were transferred to the doff tube and randomly divided into four groups: DMEM static group, DMEM electrical stimulation group, bupivacaine static group, 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: There was no significant difference in the degree of mitochondrial swelling and ROS generation in the DMEM electrical stimulation group compared with 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 the damage of myocardial mitochondria during clinical bupivacaine poisoning.