首页|右美托咪定减轻大鼠丙泊酚输注综合征的研究

右美托咪定减轻大鼠丙泊酚输注综合征的研究

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目的 探讨右美托咪定对大鼠丙泊酚输注综合征所致器官损伤的保护机制.方法 选取健康雄性SD大鼠18只,8~10周龄,体重250~280 g,采用随机数字法分为空白对照组(C组)、丙泊酚组(P组)及右美托咪定组(D组),三组大鼠分别尾静脉输注生理盐水、丙泊酚、右美托咪定+丙泊酚.每组于T0、T6、T12取大鼠颈动脉血检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、尿素氮(BUN)、肌酐(Cr)、肌钙蛋白I(cTn-I)水平;各组输注完成后取大鼠心肌组织,行HE染色观察心肌结构变化,ELISA法检测心肌组织线粒体呼吸链复合体Ⅱ活性、细胞色素C、肉碱棕榈酰转移酶I(CPT-I)、丙二酰辅酶A(Malonyl-CoA)表达量.结果 与C组相比,P组T6、T12时ALT、AST、CK、CK-MB、BUN、cTn-I水平均升高;D组T6及T、2时ALT、AST、CK、CK-MB、BUN、Cr水平均升高,D组T6时cTn-I升高(P<0.05).与 P 组相比,D 组 T6 及 T12 时 ALT、AST、CK、cTn-I 水平均下降,T12 时 CK-MB、BUN水平下降(P<0.05).P组心肌纤维排列紊乱,细胞水肿,溶解,少量散在炎细胞浸润;D组心肌纤维排列较P组规则整齐.与C组相比,P组、D组呼吸链复合体Ⅱ活性下降,Cyt-C、CPT-I、Malonyl-CoA表达均降低(P<0.05);与P组相比,D组复合体Ⅱ活性增加,Cyt-C、CPT-I、Malo-nyl-CoA表达水平升高(P<0.05).结论 右美托咪定可减轻大鼠丙泊酚输注综合征所致器官损伤,其机制可能与减轻线粒体内呼吸链的功能损害及改善脂肪酸分解代谢相关.
Study of dexmedetomidine alleviating propofol infusion syndrome in rats
Objective To investigate the protective mechanism of dexmedetomidine on organ damage in-duced by propofol infusion syndrome in rats.Methods 18 healthy male SD rats,aged 8~10 weeks and weighing 250~280 g were randomly divided into control group(Group C),propofol group(Group P)and dexmedetomidine group(Group D).The rats in each group were infused with saline,propofol and dexme-detomidine+propofol in the tail vein,respectively.In each group,blood serum samples were collected from the carotid artery of the rats at T0,T6,and T12 to measure the levels of ALT,AST,CK,CK-MB,BUN,Cr and cTn-I.Myocardial tissues from the rats were collected after the infusion was completed in each group.The tissues were stained with HE staining to observe the structural changes of the myocardi-um.The activity of mitochondrial respiratory complex Ⅱ,cytochrome C,CPT-I and Maltomide were de-tected in the cardiac muscle tissues using the ELISA method.Results Compared with group C,the levels of ALT,AST,CK,CK-MB,BUN and cTn-I in group P were increased at T6 and T12;The levels of ALT,AST,CK,CK-MB,BUN and Cr were increased at T6 and T12 in group D,and cTn-I was increased at T6 in group D(P<0.05).Compared with group P,the levels of ALT,AST,CK and cTn-I in group D were decreased averagely at T6 and T12,and the levels of CK-MB and BUN were decreased at T12(P<0.05).The results suggested that group P had disordered myocardial fibre arrangement,with cell oedema,lysis and scattered inflammatory cell infiltration.In contrast,group D had a more regular and neat myo-cardial fibre arrangement.Compared with group C,the activity of respiratory chain complex Ⅱ and the ex-pression of Cyt-C,CPT-I and Malonyl-CoA were decreased in group P and D(P<0.05).Compared with group P,the activity of complex Ⅱ and the expression levels of Cyt-C,CPT-I and Malonyl-CoA were in-creased in group D(P<0.05).Conclusion Dexmedetomidine attenuates the organ damage induced by propofol infusion syndrome in rats and the mechanism may be related to attenuation of mitochondrial respiratory chain dysfunction and improvement in fatty acid catabolism.

propofol infusion syndromemyocardial injurydexmedetomidinemitochondrial functionre-spiratory chain

孙金辉、何毕晨、顾冰蕊、刘兆媛、王婷

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新疆医科大学第三临床医学院,乌鲁木齐 830011

新疆医科大学附属肿瘤医院麻醉与围术期医学中心,乌鲁木齐 830011

丙泊酚输注综合征 心肌损伤 右美托咪定 线粒体功能 呼吸链

新疆维吾尔自治区自然科学基金青年基金项目

2021D01C413

2024

新疆医科大学学报
新疆医科大学

新疆医科大学学报

CSTPCD
影响因子:0.76
ISSN:1009-5551
年,卷(期):2024.47(6)