摘要
目的评价七氟醚对大鼠局灶性脑缺血再灌注损伤的保护作用及其机制。方法雄性 SD 大鼠24只,随机分为假手术组、损伤组、七氟醚组,每组8只。采用大脑中动脉线栓法阻断前脑血供3h、再灌注24h 制备大鼠局灶性脑缺血再灌注损伤模型。七氟醚组于再灌注前30min 经面罩吸入七氟醚(呼气末浓度维持1.0MAC,持续30min)。再灌注24h 时用 Zea Longa 评分法进行神经功能缺陷评分,并测定体重。再灌注24h 时用原位末端脱氧核苷酸转移酶标记法测定纹状体神经细胞凋亡,计算神经细胞凋亡密度,并用免疫组织化学法测定纹状体 PKCγ蛋白的表达。结果与缺血前比较,再灌注24h 时损伤组体重减轻(P＜0.01)；与假手术组比较,再灌注24h 时损伤组和七氟醚组神经功能缺陷评分及神经细胞凋亡密度增加,七氟醚组纹状体 PKCγ表达降低；与损伤组比较,七氟醚组神经功能缺陷评分、纹状体神经细胞凋亡密度降低,PKCγ表达增加(P＜0.05或0.01)。结论吸入1.0MAC 七氟醚对大鼠局灶性脑缺血再灌注损伤产生保护作用,其机制与上调纹状体 PKCγ蛋白表达有关。
Objective To investigate the protective effect of sevoflurane on the brain against focal ischemia-reperfusion （I/R） injury and its mechanism. Methods Twenty-four male SD rats weighing 250-300 g were randomly allocated into 3 groups （ n ： 8 each） ： group Ⅰ sham operation; grouop Ⅱ I/R and group Ⅲ I/R ＋ sevoflurane. The rats were anesthetized with intraperitoneal chloral hydrate 300 mg ·kg^-1 . Middle cerebral artery occlusion （MCAO） was produced by insertion of a 4-0 mono-filament nylon thread with rounded tip at bifurcation of right common carotid artery into internal carotid artery. The nylon thread was advanced cranially until resistance was felt. The depth of insertion was 18-20 mm. After 3 h MCAO the thread was withdrawn to allow reperfusion. In group m the animals inhaled 1.0 MAC sevoflurane for 30 min at 30 min before reperfusion. The rectal temperature of the animals was kept at 36.5-37.5℃ . At the end of 24 h reperfusion the animals were weighed again. The animals＇ neurological deficit was evaluated using Zea Longa score （0 = no deficit, 4 = unable to walk and unconscious）. The animals were then killed. The neuronal apoptosis in striatum was assessed （TUNEL） and the PKC protein expression in striatum was determined by immunocyto-chemistry. Results The body weight of the animals in I/R group was significantly reduced after 24h reperfusion as compared to the body weight before ischemia （P 〈 0.01 ）, while in control group and sevoflurane group there was no significant difference in the body weight before and after sham operation or I/R. The neurological deficit scores were significantly higher in I/R group than in sevoflurane group. The number of apoptotic neurons in striatum was significantly higher in I/R group than in sevoflurane group. The PKC expression in striatum was significantly higher in sevoflurane group than in I/R group （P 〈 0.01 ）. Conclusion 1.0 MAC sevoflurane inhalation has protective effect on the brain against I/R injury. Upregulation of PKC expression in striatum decreased by I/R is involved in the mechanism.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2006年第1期65-67,共3页
Chinese Journal of Anesthesiology
