右美托咪定致家兔窦性心动过缓模型中心脏窦房结Cx45和Cx31.9基因表达的变化

发布时间：2017-12-27 09:50

本文关键词：右美托咪定致家兔窦性心动过缓模型中心脏窦房结Cx45和Cx31.9基因表达的变化　出处：《临床麻醉学杂志》2017年08期 　论文类型：期刊论文

【摘要】：目的观察右美托咪定致家兔窦性心动过缓模型中心脏窦房结中缝隙连接基因蛋白Cx45和Cx31.9表达量的变化,探讨右美托咪定致心脏传导减慢的作用是否与缝隙连接基因蛋白的表达量改变有关。方法成年健康新西兰家兔48只,随机均分为三组,通过耳源静脉注射右美托咪定制备家兔窦性心动过缓模型。戊巴比妥钠基础麻醉后,迅速完成心电图、血压监测的基本操作。C组持续泵注生理盐水,D1组泵入右美托咪定10μg/kg负荷量10min,持续泵注量5μg·kg~(-1)·h~(-1)输入50min,D2组泵入右美托咪定60μg/kg负荷量10min,持续泵注量30μg·kg~(-1)·h~(-1)输入50min,观察结束后迅速开胸取出心脏准确分离心脏窦房结组织,通过免疫组化法检测Cx45、Cx31.9蛋白平均光密度,通过实时荧光定量法检测Cx45、Cx31.9基因相对表达量变化。结果 Cx45基因相对表达量D2组明显多于C、D1组(P0.05);蛋白平均光密度的改变与之一致;Cx31.9基因相对表达量D1组比C组显著增加(P0.05),D2组与C组、D1组与D2组差异无统计学意义,蛋白平均光密度的改变与之一致。结论右美托咪定使家兔窦房结低导电性缝隙连接基因蛋白Cx45、Cx31.9的表达增加,缝隙连接基因蛋白表达的变化是导致窦房结区的传导速度减慢原因之一。
[Abstract]:Objective To observe the expression of gap junction gene protein Cx45 and Cx31.9 in the central visceral sinus node of rabbits with sinus bradycardia induced by dexmedetomidine, and to explore whether the effect of dexmedetomidine on cardiac conduction slows down is related to the change of expression of gap junction gene protein. Methods 48 adult healthy New Zealand rabbits were randomly divided into three groups. The rabbit sinus bradycardia was prepared by injection of right metoami into the ear source vein. After the basic anesthesia of pentobarbital sodium, the basic operation of electrocardiogram and blood pressure monitoring was completed quickly. In group C, continuous infusion of normal saline, group D1 infusion of dexmedetomidine 10 g/kg loading dose 10min, continuous infusion of 5 g kg~ (-1) - h~ (-1) 50min input, group D2 infusion of dexmedetomidine 60 g/kg loading dose 10min, continuous infusion amount of 30 g kg~ (-1) - h~ (-1) input 50min, observed after thoracotomy quickly remove the heart accurate separation of sinoatrial node tissue by immunohistochemical method to detect Cx45 and Cx31.9 protein in the average optical density, by real-time fluorescent quantitative assay of Cx45, Cx31.9 gene mRNA expression. The relative expression levels of Cx45 mRNA in D2 group was significantly higher than C and D1 group (P0.05); the average optical density of the protein changes consistent with the relative amount of D1; the expression of Cx31.9 gene were significantly higher than C group (P0.05), no statistical significance of D2 group and C group, D1 group and D2 group were consistent, average dense protein the degree of change and. Conclusion dexmedetomidine increases the expression of low conductive gap junction protein Cx45 and Cx31.9 in sinoatrial node of rabbits, and the change of gap junction protein expression is one of the reasons leading to slow conduction velocity in sinoatrial node region.
【作者单位】：贵州医科大学麻醉学院;贵州医科大学附属医院麻醉科;
【基金】：贵州省科技厅省校合作计划项目(黔科合LH字[2015]7438)
【分类号】：R-332;R614
【正文快照】： 右美托咪定广泛用于临床麻醉及ICU镇静,但有诱发窦性心动过缓的不良反应,右美托咪定致心脏负性频率和负性传导的作用引心脏停搏的潜在危险已有多篇文献报道[1],目前研究可以明确的是右美托咪定通过抑制交感神经活动诱发迷走神经占优势及直接增加中枢迷走神经张力的情况下产生

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