Wang D, Wu X, Zhou Y, Shan G, Hu X, Li J, Liu Y, Qin X, Wang G, Xia Z
Department of Anesthesiology, First School of Clinical Medicine, Beijing Medical University, Beijing 100034, China.
Chin Med J (Engl). 1998 Oct;111(10):885-90.
To determine whether lidocaine can improve the cerebral protection provided by retrograde cerebral perfusion.
Sixteen mongrel dogs were placed on cardiopulmonary bypass and cooled to 20 degrees C. Retrograde cerebral perfusion was then carried out for 120 minutes, with the external jugular venous pressure kept at 3.33 kPa. Cardiopulmonary bypass was resumed, and the animals were rewarmed to 36 degrees C. The animals were divided into two groups. In the lidocaine group (n = 8), lidocaine was administrated continuously throughout the experiment. In the control group (n = 8), normal saline was given at the same rate.
In both groups, cerebral tissue creatine phosphate and adenosine triphosphate concentrations and energy charge increased by the end of hypothermic cardiopulmonary bypass, decreased continuously during retrograde cerebral perfusion, and recovered gradually after resuming cardiopulmonary bypass. Nevertheless, they recovered to significantly higher levels in the lidocaine group than in the control group (creatine phosphate: 2.44 +/- 0.53 versus 1.61 +/- 0.49 mumol/g wet weight, P = 0.006; adenosine triphosphate: 0.71 +/- 0.18 versus 0.50 +/- 0.17 mumol/g wet weight, P = 0.029; energy charge: 0.59 +/- 0.10 versus 0.48 +/- 0.09, P = 0.044) by the end of the experiment. There was no significant difference between the two groups in the cerebral tissue water content (control group: 77.6% +/- 1.9%; lidocaine group: 77.6% +/- 1.3%).
Continuous lidocaine infusion accelerates the recovery of cerebral tissue high energy phosphate contents after resuming cardiopulmonary bypass, but it has no effect on the formation of cerebral edema after retrograde cerebral perfusion.
确定利多卡因是否能改善逆行脑灌注提供的脑保护作用。
16只杂种犬接受体外循环并冷却至20℃。然后进行逆行脑灌注120分钟，颈外静脉压力维持在3.33 kPa。恢复体外循环，动物复温至36℃。动物被分为两组。利多卡因组（n = 8）在整个实验过程中持续给予利多卡因。对照组（n = 8）以相同速率给予生理盐水。
两组中，脑组织肌酸磷酸和三磷酸腺苷浓度以及能荷在低温体外循环结束时均升高，在逆行脑灌注期间持续下降，在恢复体外循环后逐渐恢复。然而，在实验结束时，利多卡因组这些指标恢复到显著高于对照组的水平（肌酸磷酸：2.44±0.53对1.61±0.49 μmol/g湿重，P = 0.006；三磷酸腺苷：0.71±0.18对0.50±0.17 μmol/g湿重，P = 0.029；能荷：0.59±0.10对0.48±0.09，P = 0.044）。两组脑组织含水量无显著差异（对照组：77.6%±1.9%；利多卡因组：77.6%±1.3%）。
持续输注利多卡因可加速体外循环恢复后脑组织高能磷酸盐含量的恢复，但对逆行脑灌注后脑水肿的形成无影响。
