【Animal Modeling】-Establishment of a rat model of myocardial cell mitochondrial injury induced by bupivacaine

  Objective: To observe the changes of mitochondrial morphology and reactive oxygen species generation in bupivacaine cardiomyocytes under electrical stimulation, and to explore the establishment of an ideal rat cardiomyocyte model of bupivacaine poisoning.

  Methods: The myocardial cells of male SD rats were freshly isolated by Langendroff apparatus, and then transferred to doff tubes after cell counting and randomly divided into four groups: DMEM static group, DMEM electrical stimulation group, bupivacaine static group, Bupiva Caine electrical stimulation group. The experiment was repeated five times. The mitochondrial morphology of cardiomyocytes was observed by transmission electron microscope, and the production of ROS was measured by multi-function microplate detector.

  Results: There was no significant difference in the degree of mitochondrial swelling and ROS generation between the DMEM electrical stimulation group and the DMEM static group (P > 0.05); however, the mitochondrial swelling degree in the bupivacaine electrical stimulation group was significantly higher than that in the bupivacaine static group group (P=0.000), and the production of ROS was also significantly increased (P<0.05).

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