孕酮对缺血/再灌注大鼠脑皮层水肿的影响

目的 :探讨孕酮 (progesterone ,PROG)对脑水肿的影响。方法 :48只大鼠随机分为 6组 :即缺血 /再灌 (I/R)组 ,二甲基亚砜 (DMSO)组 ,预防 (pretreatment)组 ,防治 (pre +posttreatment)组 ,治疗 (posttreatment)组 ,地塞米松 (DEXA)组。采用大鼠局灶性脑缺血 /再灌注 (I/R)模型 ,测定大脑中动脉阻塞 (MCAO) 2 4h后脑皮层水、钠、钾、钙含量。结果 :与DMSO组相比 ,应用PROG预防及防治组均能明显降低缺血皮层的H2 O(P <0 .0 1)、Na+ (P <0 .0 1)、Ca2 + (P <0 .0 1)含量 ,升高K+ (P <0 .0 1)含量 ,而治疗组虽能明显降低H2 O(P <0 .0 5 )、Na+ (P <0 .0 1) ,但降低Ca2 + (P >0 .0 5 )和升高K+ (P >0 .0 5 )的效果不显著。DEXA组的结果与PROG预防或防治组类似。结论

依托咪酯对大鼠脑皮层突触体内钙动力学的影响

目的观察依托咪酯对KCl诱发大鼠大脑皮层突触体内[Ca2+]i的影响,探讨依托咪酯的麻醉机制。方法分离SD大鼠大脑皮层制备突触体,50 mmol/L KCl刺激突触体去极化,以Fura-2 为Ca2+指示剂,测定不同浓度依托咪酯不同给药方式对突触体内[Ca2+]i的影响。实验分两部分,第一部分:KCl刺激前分别加入0.4、4、40、100μmol/L依托咪酯(终浓度);第二部分:KCl刺激后即刻加入4、40μmol/L依托咪酯。每个浓度均进行6次实验,均设立人工脑脊液作为对照,测定依托咪酯对去极化突触体内[Ca2+]i峰值和平台值的抑制率。结果KCl刺激前加入依托咪酯对KCl诱发突触体内[Ca2+]i升高的抑制程度呈浓度依赖性;峰值抑制率分别为5%±3%,11%±6%,24%±10%和33% ±12%。KCl刺激后即刻加入依托咪酯40 μmol/L升高突触体内[Ca2+]i平台值(P<0.05)。结论依托咪酯改变KCl诱导大鼠大脑皮层突触体内钙动力学,其作用与突触前膜上电压敏感性[Ca2+]i通道和钙移除机制有关。

慢性束缚应激对大鼠睡眠时相的影响及酸枣仁汤的干预作用

目的:探讨慢性束缚应激对大鼠睡眠结构的影响,以及酸枣仁汤的干预作用。方法:采用经典的慢性束缚应激的造模方法,复制大鼠慢性应激的模型,结合大鼠大脑皮层脑电和肌电描记技术,监测模型复制后大鼠12h脑电图(EEG)和肌电图(EMG)的变化,分析各睡眠时相的持续时间及所占睡眠总时间的比例,并探究中药复方酸枣仁汤对其干预作用。结果:从睡眠持续时间来看,与空白组相比,模型复制后大鼠在睡眠总时间、浅睡眠(LS)、慢波睡眠(SWS)以及快动眼(REM)睡眠的持续时间均显著缩短(P<0.05)。与模型组相比,酸枣仁汤给药组大鼠在睡眠总时间、LS和SWS期睡眠持续时间均显著延长(P<0.05),REM期睡眠虽有延长的趋势,但无统计学意义(P>0.05);从各睡眠时相所占睡眠总时间的比例来看,与空白组相比,模型复制后大鼠LS期所占比例显著增加(P<0.05),SWS期睡眠所占的比例则明显减小(P<0.05),而REM期所占睡眠总时间的比例与空白组相比基本持平。与模型组相比,酸枣仁汤给药组大鼠SWS期所占睡眠总时间的比例显著提高(P<0.05),LS期和REM期睡眠所占比例虽有下降的趋势,但是在统计学上无显著性差异(P>0.05)。结论:慢性束缚应激使大鼠各睡眠时相持续时间和所占睡眠总时间的比例发生明显的改变,大鼠的正常睡眠结构已被打乱,酸枣仁汤能有效对抗慢性束缚应激对大鼠睡眠结构造成的影响。

EFFECT OF ELECTROACUPUNCTURE ON NOREPINEPHRINE LEVEL AND APOPTOSIS IN CEREBRAL CORTEX TISSUE IN RATS WITH CEREBRAL ISCHEMIA-REPERFUSION

Objective: To investigate the underlying neurobiological mechanism of the protective effect of electroacupuncture (EA) during cerebral ischemia-reperfusion (CI-R). Methods: In the first part of the study, 15 SD rats were evenly randomized into control group, CI-R-48h model group and CI-R-48h+EA group. The cortical apoptosis and expression of Bcl-2 and Bax proteins in each group were detected by flow cytometer (FCM). In the second part of the study, 75 SD rats were evenly randomized into control, CI-R-3min, CI-R-3min+EA, CI-R-48h and CI-R-48h+EA groups. Cortical norepinephrine (NE) concentration was detected by fluorescence spectrometer. CI-R model was established by occlusion of the bilateral common carotid arteries and reperfusion. EA (4～16 Hz, 1～3 V) was applied to “Shuigou”(水沟 GV 26) and “Chengjiang”(承浆 CV 24) for 30 min before CI and after reperfusion respectively. Results: In the first part of this study, results indicated that the number of the apoptotic neurons and the apoptosis rate of CI-R-48h group were significantly higher than those of control group; while comparison between CI-R-48h+EA and CI-R-48h groups showed that the number of the apoptotic neurons and the apoptosis rate of the former group were significantly lower than those of the later group (P<0.05). In comparison with control group, after CI-48h, Bax expression was up-regulated significantly and Bcl-2 down-regulated markedly (P<0.05). Comparison between CI-R-48h and CI-R-48h+EA group indicated that Bax expression of the later group was significantly lower than that of the former group, while Bcl-2 expression of CI-R-48h+EA group was significantly higher than that of CI-R-48h group (P<0.05), suggesting that EA could reverse CI induced reactions of these two indexes. In the second part of the study, in comparison with control group, NE concentration in cerebral cortex of CI-R-3min group increased significantly (P<0.05); while NE content of CI-R-3min+EA group was significantly lower than that of CI-R-3min group (P<0.05). No significant difference was found between CI-R-3min group and control group in cortical NE levels; and no significant changes were found about NE levels in CI-R-48h and CI-R-48h+EA groups, suggesting that EA could inhibit the increase of cortical NE level in the early stage of CI. Conclusion: Changes of NE concentration in the cerebral cortex during the earlier period of CI-R is possibly related to the incidence of cortical apoptosis. EA can reduce the increase of NE due to CI and thus may inhibit CI-induced cortical apoptosis.