Fink B R, Aasheim G, Kish S J, Croley T S
Anesthesiology. 1975 Jun;42(6):731-6. doi: 10.1097/00000542-197506000-00017.
The kinetics of neural uptake and efflux of lidocaine hydrochloride were studies by means of a standardized technique for blocking the intraorbital nerve of the rat, using a palatal jig. Following injection of 14-C-labeled local anesthetic, groups of ten animals were saccraficed at incipient recovery from sensory block or at othertimes. The nerves were weighed and assayed for radioactivity. The lengths of nerve containing high levels of lidocaine varied inversely with the times elapsed since onset of block. In experiments where a fixed quantity (2 mg) drug was injected, the incidence of block 2 hours later was concentrated-dependent, occuring in 80 per cent of animals after 2 per cent, in 40 per cent after 1 per cent, and in none after 0.5 per cent lidocaine. Epinephrine, 1:200,000, prolonged by 80 per cent the block effected with 0.2 ml of 1 per cent lidocaine. At the onset of recovery the neural contents of lidocaine at the sites of injection were 484 plus or minus 404 ng/mg of nerve in epinephrine-treated nerves, and 274 plus or minus 218 ng/mg in nonepinephrine-treated nerved (N.S., P greater than 0.05). Quantitative comparisons of in-vivo effectiveness of local anesthetic solutions can be made with this technique.
采用一种标准化技术,使用腭夹阻断大鼠眶内神经,研究了盐酸利多卡因的神经摄取和流出动力学。注射14-C标记的局部麻醉剂后,在感觉阻滞开始恢复时或其他时间,每组十只动物被处死。称取神经重量并测定放射性。含有高浓度利多卡因的神经长度与阻滞开始后的时间呈反比。在注射固定量(2毫克)药物的实验中,2小时后的阻滞发生率呈浓度依赖性,2%利多卡因后80%的动物出现阻滞,1%后40%出现阻滞,0.5%利多卡因后无动物出现阻滞。1:200,000的肾上腺素使0.2毫升1%利多卡因产生的阻滞时间延长80%。在恢复开始时,肾上腺素处理的神经中注射部位的利多卡因神经含量为484±404纳克/毫克神经,未用肾上腺素处理的神经中为274±218纳克/毫克神经(无显著性差异,P>0.05)。用这种技术可以对局部麻醉溶液的体内有效性进行定量比较。