摘要
目的研究七氟烷后处理(SevoPoC)对心肌缺血再灌注损伤(MIRI)的保护作用及与钠钙交换体1(NCX1)的相关性。方法取36只SD大鼠,构建离体心脏灌注模型,待血流动力学稳定0.5h后,缺血0.5h复灌1h构建大鼠MIRI模型,随机分为对照组(离体心脏灌注KH液2h)、模型组(离体心脏灌注KH液0.5h,停止灌注0.5h,接着恢复灌注1h)和实验组(复灌即刻用3%的七氟烷持续灌注15min,其他同模型组),三组各12只。比较三组大鼠平衡灌注期(T0)、再灌注0.5h(T1)和再灌注1h(T2)各项心功能指标的变化情况,采用免疫印迹法检测三组大鼠NCX1、兰尼碱受体2(RyR2)及L型钙通道(LTCCs)蛋白的表达水平,并用实时荧光定量PCR法检测大鼠NCX1、RyR2及LTCCsmRNA的相对表达量。结果相比T0,模型组再灌注0.5h(T1)和再灌注1h(T2)左心室舒张末期压力(LVEDP)显著增高(P<0.05),而最大左心室发展压下降速率(-dp/dt)、最大左心室发展压上升速率(+p/dt)、心率与左心室发展压的乘积(RPP)显著下降(P<0.05);相比对照组,模型组T1和T2时LVEDP显著增高(P<0.05),而-dp/dt、+dp/dt和RPP显著下降(P<0.05);相比T0,实验组T1和T2时LVEDP显著增高(P<0.05),T1和T2时LVEDP较对照组明显增高,而较模型组显著下降(P<0.05);实验组T1时-dp/dt较模型组显著增高(P<0.05),T2时-dp/dt较T0显著下降,亦较对照组显著下降(P<0.05);实验组T1和T2时+dp/dt和RPP较模型组显著增高(P<0.05)。三组大鼠RyR2和LTCCs蛋白表达水平的比较,无显著差异(P>0.05);模型组大鼠NCX1蛋白表达水平较对照组明显升高(P<0.05),而实验组大鼠NCX1蛋白表达水平较模型组明显下降(P<0.05)。三组大鼠NCX1、RyR2及LTCCsmRNA相对表达量的比较,无显著差异(P>0.05)。结论SevoPoC可促进MIRI大鼠心功能恢复,其具有保护MIRI的作用,而这一保护作用可能与其具有抑制NCX1表达的作用密切相关。
Objective To study the protective effect of sevoflurane postconditioning (SevoPoC) on myocardial ischemia-reperfusion injury (MIRI) and its correlation with Na^+- Ca^ 2+ exchanger isoform 1 (NCX1). Methods Thirty-six SD rats were randomly divided into control group (isolated heart perfusion of KH solution for 2 h),model group (isolated heart perfusion of KH solution for 0.5 h,stop perfusion for 0.5 h, then resume perfusion for 1 h) and experimental group (reperfusion immediately with 3% sevoflurane for 15 min,other same model group),with 12 rats in each group. The expression levels of NCX1,ryanodine receptor 2 (RyR2) and L-type Ca^ 2+ channels (LTCCs) proteins in three groups of rats at different time points were detected by immunoblotting,and the relative expression levels of NCX1,RyR2 and LTCCs were detected by real-time fluorescence quantitative PCR. Results Compared with T0,the left ventricular end-diastolic pressure (LVEDP) increased significantly at 0.5 h (T1) and 1 h (T2) reperfusion in model group ( P <0.05). While the maximum left ventricular developed pressure decrease rate (-dp/dt),the maximum left ventricular developed pressure increase rate (+p/dt),and heart rate × left ventricular developed pressure (RPP) decreased significantly at T1 and T2 in model group ( P <0.05). Compared with the control group,the LVEDP of the model group increased significantly at T1 and T2 ( P <0.05),but decreased significantly at -dp/dt,+dp/dt and RPP ( P <0.05). Compared with T0,the LVEDP of the experimental group increased significantly at T1 and T2 ( P <0.05),and decreased significantly at T1 and T2 ( P <0.05);at T1,the -dp/dt of the experimental group increased significantly compared with the model group ( P <0.05),and at T2,the -dp/dt of the experimental group was significantly higher than that of the model group ( P <0.05). The decrease was also significantly lower than that of the control group ( P <0.05),and the +dp/dt and RPP in the experimental group at T1 and T2 were significantly higher than those in the model
作者
陈晓芳
赵晓亮
王涛
徐志新
CHEN Xiao-fang;ZHAO Xiao-liang;WANG Tao(Department of Anesthesiology,The Second Affiliated College of Hainan Medical University,Haikou Hainan 570100,China;Department of Anesthesiology,People's Hospital of Xinjiang Uygur Automonous Regeion,Urumqi Xinjiang 830001,China)
出处
《临床和实验医学杂志》
2019年第13期1359-1363,共5页
Journal of Clinical and Experimental Medicine
基金
海南省医药卫生科研项目(编号:1801032021A2001)
关键词
大鼠
心肌缺血再灌注损伤
七氟烷后处理
心功能
钠钙交换体1
兰尼碱受体2
L型钙通道
Rats
Myocardial ischemia-reperfusion injury
Sevoflurane postconditioning
Cardiac function
Sodium-calcium exchanger 1
Lanine receptor 2
L-type calcium channel
