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目的:观察利多卡因能否改善逆行脑灌注的脑保护作用。方法:16只杂种犬接受体外循环并降温至20C,停循环,逆行脑灌注120分钟,恢复体外循环并复温至36℃。利多卡因组(n=8)实验期间持续给予利多卡因(4mg·kg~(-1)后0.2mg·kg~(-1)·min~(-1),逆行脑灌注期间为0.5mg·min~(-1));对照组(n=8)则给予等量生理盐水。结果:实验末利多卡因组脑组织磷酸肌酸、三磷酸腺苷含量和能量指数均明显高于对照组(分别为磷酸肌酸:2.44±0.53比1.61±0.49μmol/gwetw,P<0.01;三磷酸腺苷:0.71±0.18比0.50±0.17μmol/gwetw,P<0.05;能量指数:0.59±0.10比0.48±0.09,P<0.05)。但两组间脑组织丙二醛含量无显著差异。结论:围逆行脑灌注期间持续给予利多卡因改善脑保护作用,可能与恢复体外循环后犬脑组织高能磷酸盐含量增加有关。
Objective: To observe whether lidocaine can improve brain protective effect of retrograde cerebral perfusion. Methods: 16 hybrid dogs were subjected to cardiopulmonary bypass and cooled to 20 ° C. Cardioplegia and retrograde cerebral perfusion were performed for 120 minutes to resume cardiopulmonary bypass and rewarmed to 36 ° C. During lidocaine group (n = 8), lidocaine (0.2 mg · kg -1 -1 min -1) was given continuously after the infusion of lidocaine (0.5 mg · Min ~ (-1)). The control group (n = 8) received the same amount of normal saline. Results: At the end of the experiment, the contents of phosphocreatine phosphorylate, adenosine triphosphate and energy index in the brain of the lidocaine group were significantly higher than those of the control group (creatine phosphorylation: 2.44 ± 0.53 vs 1.61 ± 0.49μmol / gwetw, P <0.01; adenosine triphosphate: 0.71 ± 0.18 vs 0.50 ± 0.17 μmol / gwetw, P <0.05; energy index: 0.59 ± 0.10 vs. 0.48 ± 0.09, P <0.05). However, there was no significant difference in MDA content between the two groups. CONCLUSION: Lidocaine may improve cerebral protection during peri-perfusion of cerebral perfusion, which may be related to the increase of high-energy phosphate content in canine brain tissue after cardiopulmonary bypass.