Department of Prosthodontics, Semmelweis University, Budapest, Hungary.
Department of Pedodontics and Orthodontics, Semmelweis University, Budapest, Hungary.
Brain Res Bull. 2017 Oct;135:157-162. doi: 10.1016/j.brainresbull.2017.10.011. Epub 2017 Oct 18.
Since a significant proportion of diabetic patients have clinical or subclinical neuropathy, there may be concerns about the use of local anaesthetics. The present study was designed to determine and compare the effects of articaine, a widely used anaesthetic in dental practice, and lidocaine on the resting and axonal stimulation-evoked release of [H]noradrenaline ([H]NA) in prefrontal cortex slices and the release of [H]NA in spinal cord slices prepared from non-diabetic and streptozocin (STZ)-induced diabetic (glucose level=22.03±2.31mmol/l) rats. The peak of allodynia was achieved 9 weeks after STZ-treatment. Articaine and lidocaine inhibited the stimulation-evoked release in a concentration-dependent manner and increased the resting release by two to six times. These effects indicate an inhibitory action of these anaesthetics on Na- and K-channels. There was no difference in clinically important nerve conduction between non-diabetic and diabetic rats, as measured by the release of transmitter in response to axonal stimulation. The uptake and resting release of NA was significantly higher in the brain slices prepared from diabetic rats, but there were no differences in the spinal cord. For the adverse effects, the effects of articaine on K channels (resting release) are more pronounced compared to lidocaine. In this respect, articaine has a thiophene ring with high lipid solubility, which may present potential risks for some patients.
由于相当一部分糖尿病患者存在临床或亚临床神经病变,因此可能会对局部麻醉剂的使用产生担忧。本研究旨在确定并比较在牙科实践中广泛使用的麻醉剂阿替卡因和利多卡因对来自非糖尿病和链脲佐菌素(STZ)诱导的糖尿病(血糖水平=22.03±2.31mmol/l)大鼠前额叶皮层切片中[H]去甲肾上腺素([H]NA)的静息和轴突刺激诱发释放以及脊髓切片中[H]NA释放的影响。在 STZ 处理后 9 周达到所有感觉过敏的峰值。阿替卡因和利多卡因以浓度依赖性方式抑制刺激诱发的释放,并将静息释放增加两到六倍。这些作用表明这些麻醉剂对 Na 和 K 通道具有抑制作用。通过轴突刺激释放来测量,在非糖尿病和糖尿病大鼠之间,没有观察到临床重要的神经传导差异。与糖尿病大鼠相比,脑切片中 NA 的摄取和静息释放显著增加,但脊髓中没有差异。对于不良反应,阿替卡因对 K 通道(静息释放)的影响比利多卡因更为明显。在这方面,阿替卡因具有高脂溶性的噻吩环,这可能对某些患者构成潜在风险。