背景:室性心律失常通常是由交感神经过度引起的急性心肌缺血引起的,并且通常对抗心律失常疗法产生抗性。据报道,胸部硬膜外麻醉可以终止致命的室性心律失常;然而,其潜在的机制是未知的。
方法:大鼠随机分为4组:假加布比卡因,缺血/再灌注(IR),和IR加布比卡因组。布比卡因(1mg/mL,在建立心肌缺血/再灌注大鼠模型之前,将0.05mL/100g体重)鞘内注射到L5-L6椎间隙中。此后,心律失常,心功能,心肌损伤,评估心脏和脊髓的电活动。
结果:鞘内注射布比卡因抑制脊髓神经活动,改善心率变异性,室性心律失常评分降低,改善IR大鼠心功能不全。此外,鞘内注射布比卡因减轻心肌损伤和心肌细胞凋亡,调节心肌细胞自噬和连接蛋白-43的分布。
结论:我们的结果表明,鞘内注射布比卡因可以减弱脊髓神经活动,以防止IR引起的心律失常和功能障碍,这种抗心律失常活性可能与调节自主神经平衡有关,心肌细胞凋亡和自噬,和心脏缝隙连接功能。
BACKGROUND: Ventricular arrhythmia is commonly provoked by acute cardiac ischemia through sympathetic exaggeration and is often resistant to anti-arrhythmic therapies. Thoracic epidural anesthesia has been reported to terminate fatal ventricular arrhythmia; however, its underlying mechanism is unknown.
METHODS: Rats were randomly divided into four groups: sham, sham plus bupivacaine, ischemia/reperfusion (IR), and IR plus bupivacaine groups. Bupivacaine (1 mg/mL, 0.05 mL/100 g body weight) was injected intrathecally into the L5-L6 intervertebral space prior to establishing a myocardial IR rat model. Thereafter, cardiac arrhythmia, cardiac function, myocardial injury, and electrical activities of the heart and spinal cord were evaluated.
RESULTS: Intrathecal bupivacaine inhibited spinal neural activity, improved heart rate variability, reduced ventricular arrhythmia score, and ameliorated cardiac dysfunction in IR rats. Furthermore, intrathecal bupivacaine attenuated cardiac injury and myocardial apoptosis and regulated cardiomyocyte autophagy and connexin-43 distribution during myocardial IR.
CONCLUSIONS: Our results indicate that intrathecal bupivacaine blunts spinal neural activity to prevent cardiac arrhythmia and dysfunction induced by IR and that this anti-arrhythmic activity may be associated with regulation of autonomic balance, myocardial apoptosis and autophagy, and cardiac gap junction function.