摘要
BACKGROUND： It is known that intravenous anesthetic etomidate fat emulsion has cerebral protection. Now many scholars focus on the research of its cerebral protection from molecular biology, but the mechanism of cerebral protection is still fully unclear. OBJECTIVE： To observe the influence of etomidate fat emulsion on the [Ca^2＋]i in hippocampal neurons during the transient cerebral ischemia injury in rats. DESIGN： Randomized controlled observation. SETTING： Weifang Medical College. MATERIALS： This study was carried out in the functional laboratory of Weifang Medical College between October 2005 and March 2006. Twenty-four male healthy Wistar rats, aged 3 to 4 months, were involved. Etomidate fat emulsion was provided by the limited company of En-hua Medical Bloc in Jiangsu Province （code of H200205l l） and the other agents and materials were provided by Laboratory Center of Weifang Medical College. METHODS： The 24 Wistar rats were randomized into 3 groups： sham-operation group, model group and etomidate preconditioning group, with 8 rats in each. Rat models of transient cerebral ischemia injury were made by the ligation of bilateral carotid arteries combined with descending blood pressure in the latter two groups. Before ischemia （ligation of bilateral common carotid artery）, rats in the etomidate preconditioning group were intraperitoneally injected with 12 mg/kg etomidate fat emulsion and then persistently intraperitoneally injected with etomidate fat emulsion at 1.0 mg/kg per minute. Rats in the model group were not administrated. Rats in the sham-operation group were only performed bilateral common carotid artery isolation. When rats were modeled, their brain tissues were quickly taken out and detected. MAIN OUTCOME MEASURES： Change of the fluorescence pixel value of the [Ca^2＋]i in each group by the laser scanning confocal microscope. RESULTS： Twenty-four rats were involved in the final analysis. Fluorescence pixel value in the sham-operation group was in the low level. Fluorescence pixel value in the model group was significantly higher than that in the sham-operation group （P 〈 0.01）. Fluorescence pixel value in the etomidate preconditioning group was significantly lower than that in the model group （P 〈 0.01 ）. CONCLUSION： The protection of etomidate fat emulsion to the transient cerebral ischemic injury in rats is associated with the inhibition to the increase of [Ca^2＋]i to some extent.
BACKGROUND： It is known that intravenous anesthetic etomidate fat emulsion has cerebral protection. Now many scholars focus on the research of its cerebral protection from molecular biology, but the mechanism of cerebral protection is still fully unclear. OBJECTIVE： To observe the influence of etomidate fat emulsion on the [Ca^2＋]i in hippocampal neurons during the transient cerebral ischemia injury in rats. DESIGN： Randomized controlled observation. SETTING： Weifang Medical College. MATERIALS： This study was carried out in the functional laboratory of Weifang Medical College between October 2005 and March 2006. Twenty-four male healthy Wistar rats, aged 3 to 4 months, were involved. Etomidate fat emulsion was provided by the limited company of En-hua Medical Bloc in Jiangsu Province （code of H200205l l） and the other agents and materials were provided by Laboratory Center of Weifang Medical College. METHODS： The 24 Wistar rats were randomized into 3 groups： sham-operation group, model group and etomidate preconditioning group, with 8 rats in each. Rat models of transient cerebral ischemia injury were made by the ligation of bilateral carotid arteries combined with descending blood pressure in the latter two groups. Before ischemia （ligation of bilateral common carotid artery）, rats in the etomidate preconditioning group were intraperitoneally injected with 12 mg/kg etomidate fat emulsion and then persistently intraperitoneally injected with etomidate fat emulsion at 1.0 mg/kg per minute. Rats in the model group were not administrated. Rats in the sham-operation group were only performed bilateral common carotid artery isolation. When rats were modeled, their brain tissues were quickly taken out and detected. MAIN OUTCOME MEASURES： Change of the fluorescence pixel value of the [Ca^2＋]i in each group by the laser scanning confocal microscope. RESULTS： Twenty-four rats were involved in the final analysis. Fluorescence pixel value in the sham-operation group was in the low level. Fluorescence pixel value in the model group was significantly higher than that in the sham-operation group （P 〈 0.01）. Fluorescence pixel value in the etomidate preconditioning group was significantly lower than that in the model group （P 〈 0.01 ）. CONCLUSION： The protection of etomidate fat emulsion to the transient cerebral ischemic injury in rats is associated with the inhibition to the increase of [Ca^2＋]i to some extent.
