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作 者:张军[1] 庄心良[1] 赵新峰[1] 李士通[1] 王莹恬[1]
机构地区:[1]上海交通大学附属上海第一人民医院麻醉科,200080
出 处:《中华麻醉学杂志》2005年第9期682-684,共3页Chinese Journal of Anesthesiology
摘 要: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。Objective To study the effect of etomidate on the changes in [Ca^2+]i in rat cerebrocortical synaptosomes induced by KCl. Methods Freshly isolated SD rat cerebrocortical synaptosomes were prepared. KCl was used as chemical stimulant. Neurochemical method was employed (Fura-2 was used as calcium indicator). Etomidate was added (the end concentration was 0.4, 4, 40 and 100 μmol·L^-1 respectively) before and after stimulation with KCl 50 mmol·L^-1 to determine the peak and plateau [Ca^2+]i in the cerebrocortical synaptomes. Results Before KCl stimulation etomidate inhibited KCl-evoked increase in intra-synaptosomal [Ca^2+]i in a concentration-dependent manner. The inhibitory ratio of peak calcium concentration was 5%±3%, 11%±6%, 24%±10% and 33%±12% respectively as compared with control. Etomidate at concentration of 40 μmol·L^-1 and above had significant effect on [Ca^2+]i. When added immediately after KCl stimulation, 4, 40 μmol·L^-1 etomidate significantly increased plateau [Ca^2+]i in synaptosomes. Conclusion Etomidate alters KCl-induced calcium dynamics in rat cerebrocortical synaptosomes. Presynaptic calcium channels and calcium removal mechanism are involved in its anesthetic action.
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