Abstract
BackgroundElectroacupuncture is well known for its advantageous neuroanalgesic and therapeutic effects on myocardial ischemia–reperfusion injury. The purpose of the present research was to verify whether electroacupuncture can alleviate bupivacaine-induced myocardial injury.MethodsSpecific pathogen-free Wistar rats were used to establish the bupivacaine-induced myocardial injury model. Western blot, PCR, transmission electron microscope and enzyme-linked immunosorbent (ELISA) methods were used to evaluate bupivacaine-induced structure injury and dysfunction of the mitochondria as well as the alleviating effects of lipid emulsion, acupoint injection, and electroacupuncture pre-treatment of the oxidase stress response.ResultsBupivacaine caused structural damage, degradation, and swelling of mitochondria. Furthermore, it reduced adenosine triphosphate (ATP) synthesis and impaired energy metabolism in the mitochondria. Structural and functional impairment of the mitochondria was alleviated via lipid emulsion injection, acupoint injection, and electroacupuncture pre-treatment. Electroacupuncture pre-treatment of PC6 yielded a greater alleviating effect than others approaches. Following electroacupuncture pre-treatment of PC6 point, the number of mitochondria increased; apoptosis was reduced, enzymatic activity of cytochrome C oxidase (COX) and superoxide dismutase and expression of uncoupling protein 2, voltage-dependent anion channel 1, and Bcl 2 were upregulated and SLC25A6, MDA levels were downregulated. Additionally, our findings indicated that electroacupuncture pre-treatment of PC6 point exerted an effect on the mitochondria via the mitochondrial-transcription-factor-A/nuclear-respiratory-factor-1/proliferator-activated-receptor-gamma-coactivator-1 pathway.ConclusionThe present study revealed that electroacupuncture pre-treatment of PC6 could effectively alleviate bupivacaine-induced myocardial mitochondrial damage, thereby providing a theoretical basis for clinical studies and applications of this treatment method.
Highlights
Electroacupuncture is well known for its advantageous neuroanalgesic and therapeutic effects on myocardial ischemia–reperfusion injury
Materials The primary materials used in the present study were as follows: fetal bovine serum (FBS), bupivacaine, lipid emulsions, puerarin injections, pentobarbital sodium, the RNeasy Mini Kit (QIAGEN), the QuantiNova SYBR Green PCR Kit (QIAGEN), the QuantiNova Reverse Transcription Kit (QIAGEN), Anti-Uncoupling protein 2 (UCP2) (GeneTex), Anti-NRF1 (GeneTex), Anti-ADP/ATP translocase 3 (SLC25A6) (GeneTex), AntimtTFA (GeneTex), Anti-Voltagedependent anion channel 1 (VDAC1), Anti-PGC-1 (Abcam), Anti-Bcl-2 (Abcam) and adenosine triphosphate (ATP) assay kit (Abcam, ab83355)
Protective effect of different treatments on bupivacaine‐induced myocardial injury Previous studies have demonstrated that EA pre-treatment exerts an alleviating effect on bupivacaine-induced toxicity [8]
Summary
Electroacupuncture is well known for its advantageous neuroanalgesic and therapeutic effects on myocardial ischemia–reperfusion injury. Local anesthesia can lead to complications, resulting in inevitable adverse effects. Local anesthesia affects the central nervous system and the cardiovascular system and may lead to neurotoxicity [2], resulting in nerve injuries and. Deaths from local anesthesia are mainly attributed to adverse effects on the cardiovascular system, which include contractile dysfunction and cardiac arrhythmia [3], and are mainly characterized by hemodynamic changes [4]. For every 1000 peripheral nerve blocks, 0.04 to 1.8 cases of myocardial toxicity are likely to occur, leading to severe symptoms [6]. Bupivacaine-induced cardiotoxicity may result in cardiac arrhythmia, poor myocardial contractility and cardiac arrest due to circulatory collapse [7, 8]. Sztark et al reported that bupivacaine may directly inhibit mitochondrial respiratory chain complex I (MRCC-I), alter mitochondrial membrane structure, increase proton permeability in the mitochondrial inner membranes (MIMs), induce loss of mitochondrial calcium, and reduce mitochondrial membrane potential (MMP) [9], thereby affecting the respiratory function and energy production of the mitochondria and eventually leading to mitochondrial dysfunction
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