丙泊酚麻醉对创伤性脑损伤大鼠神经元再生和神经功能的影响

Effects of propofol anesthesia on neuronal regeneration and neurological function in rats with trau- matic brain injury

目的观察丙泊酚麻醉对创伤性脑损伤（TBI）大鼠的影响。方法将sD大鼠分为假手术组、模型组、丙泊酚低剂量组[36mg／（kg·h）]和丙泊酚高剂量组[72mg／（kg·h）]，每组20只。于TBI术前30min至术后1．5h静脉注射给药，观察大鼠术后的死亡率，神经功能和神经元再生状况。结果术后28d，丙泊酚低剂量组大鼠死亡率显著高于模型组大鼠死亡率，差异有统计学意义（x^2=7．648，P=0．024）；丙泊酚高剂量组大鼠死亡率显著高于模型组大鼠死亡率，差异有统计学意义（x^2=9．152，P=0．018）；在术后1—7d，模型组大鼠平均体重为（365．4±2．4）g，丙泊酚低剂量组大鼠平均体重为（347．2±2．5）g，丙泊酚高剂量组大鼠平均体重为（314．9±2．35）g，使用丙泊酚麻醉的大鼠体重均低于模型组，到终点后丙泊酚高剂量组大鼠体重显著低于模型组（t=8．363，P=0．026）；模型组大鼠进入目的洞时间显著高于假手术组（t=6．783，P=0．047）；各组大鼠经巴恩斯迷宫实验检测结果显示，大鼠进入目的洞时间假手术组为（138．3±1．5）s，模型组为（145．6±1．4）s，丙泊酚低剂量组为（144．2±1．6）s，丙泊酚高剂量组为（169．4±1．7）s，模型组大鼠进入目的洞时间显著高于假手术组（t=6．783，P=0．047），丙泊酚低剂量组与模型组比较差异无统计学意义（t=1．863，P=0．064），而丙泊酚高剂量组大鼠的时间显著长于模型组（t=9．483，P=0．014）；同时，丙泊酚低剂量组大鼠脑部神经元新生显著低于模型组（t=7．824，P=0．038），丙泊酚高剂量组大鼠脑部神经元新生显著低于模型组（t=6．575，P=0．041）。结论高剂量丙泊酚麻醉对于TBI大鼠具有恶化作用。

Objective To observe the effect of propofol anesthesia on traumatic brain injury （TBI） in rats. Methods Rats were divided into sham operation group, model group, low dose propofol group [36 mg/（ kg. h） ] and high dose propofol group [72 mg/（ kg. h） ]. Propofol was administered intra- venously from 30 min before to 1.5 h after surgery, and the mortality, neurological function and neuronal regeneration were determined. Results After 28 d, propofol in low dose group was significantly higher than the mortality of rats in the model group, the difference was statistically significant （x^2= 7.648, P= 0. 024） ; high dose of propofol in rats was significantly higher than the mortality of the rats in the model group, the difference was statistically significant （x^2 = 9. 152, P = 0. 018） ; 1 - 7 d after the operation, the average weight of the model group was （365.4 ± 2.4） g, the average weight of propofol in low dose group rats was （347. 2 ±2. 5） g, the average weight of propofol in high dose group rats was （314. 9 ±2. 35） g, using propofol anesthetized rats weight to body weight were lower than the model group, high dose of propo- fol in rats after significant end point compared with model group （ t = 8. 363, P = 0. 026 ） ; the rats in model group to hole time was significantly higher than sham operation group （ t = 6. 783, P = 0. 047） ; the rats by Barnes maze test showed that the rats to enter the hole time of sham operation group （ 138.3 ± 1.5 ） s, the model group （ 145.6 ± 1.4） s, propofol in low dose group （ 144. 2 ± 1.6） s, high dose of propofol for （169. 4 ± 1.7） s, the rats in model group to hole time was significantly higher than sham operation group （t = 6. 783, P = 0. 047 ）, no statistically significant difference between the low dose propofol group and model group （ t = 1. 863, P = 0. 064）, and high dose of propofol in rats was significantly longer than that of model group （t =9. 483, P =0. 014） ; at the same time, the use of propofol anesthesia of propofol in low dose group rat brain neurons of newborn were significantly lower than the model group （ t = 7. 824, P = 0. 038 the use of propofol anesthesia with propofol）, high dose group rat brain neurons of newborn were significantly lower than the model group （ t = 6. 575, P = 0. 041 ）. Conclusion High dose propofol anesthesia has a deteriorating effect on rats with TBI.