中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2014年
8期
675-679
,共5页
王玉华%付丽佳%王丽红%徐莲琴%杨宝峰
王玉華%付麗佳%王麗紅%徐蓮琴%楊寶峰
왕옥화%부려가%왕려홍%서련금%양보봉
心律失常%电生理学技术,心脏%膜片钳术%蛇葡萄素
心律失常%電生理學技術,心髒%膜片鉗術%蛇葡萄素
심률실상%전생이학기술,심장%막편겸술%사포도소
Arrhythmia%Electrophysiologic techniques,cardiac%Patch-clamp techniques%Ampelopsin
目的 研究蛇葡萄素抑制大鼠室性心律失常的作用及其电生理机制.方法 在体实验,成年雄性Wistar大鼠采用抓阄法随机分为生理盐水对照组(对照组)、蛇葡萄素低剂量(1 mg/kg)组、蛇葡萄素中剂量(3 mg/kg)组和蛇葡萄素高剂量(10 mg/kg)组4组.预处理后运用泵注乌头碱的方法诱发大鼠心律失常,观察蛇葡萄素对乌头碱诱导的大鼠心律失常的保护作用.离体实验,使用酶解法急性分离大鼠心室肌细胞,并应用膜片钳技术记录蛇葡萄素对大鼠心室肌细胞上钠电流(INa)、钙电流(ICa)、瞬时外向钾电流(Ito)和内向整流钾电流(IK1)等离子通道电流的影响.结果 在体实验结果显示,蛇葡萄素低、中和高剂量组大鼠实验性室性心律失常的发生率均低于对照组(n=5,P均＜0.05).体外全细胞膜片钳实验结果显示蛇葡萄素低、中和高剂量组大鼠心室肌细胞动作电位时程(APD)均大于对照组,动作电位幅值也均低于对照组[(120.1±7.4)、(113.2±9.0)和(101.8±5.1) mV比(134.1±6.9) mY,n=9,P均＜0.05].蛇葡萄素低、中和高剂量组大鼠心室肌细胞INa峰值电流密度均小于对照组[(-31.03 ±2.61)、(-26.63±3.72)和(-17.55 ±4.43)pA/pF比(-36.75±3.60)pA/pF,n=9,P均＜0.05],但4组间最大峰值电位差异无统计学意义.蛇葡萄素高剂量组IK1峰值电流密度大于对照组[(-37.47±7.32)pA/pF比(-25.26±4.13)pA/pF,n=5,P＜0.05],而ICa和Ito4组间差异则无统计学意义.结论 蛇葡萄素具有抗大鼠心律失常的作用,其电生理机制为抑制INa、增强IK1,进而延长APD.
目的 研究蛇葡萄素抑製大鼠室性心律失常的作用及其電生理機製.方法 在體實驗,成年雄性Wistar大鼠採用抓鬮法隨機分為生理鹽水對照組(對照組)、蛇葡萄素低劑量(1 mg/kg)組、蛇葡萄素中劑量(3 mg/kg)組和蛇葡萄素高劑量(10 mg/kg)組4組.預處理後運用泵註烏頭堿的方法誘髮大鼠心律失常,觀察蛇葡萄素對烏頭堿誘導的大鼠心律失常的保護作用.離體實驗,使用酶解法急性分離大鼠心室肌細胞,併應用膜片鉗技術記錄蛇葡萄素對大鼠心室肌細胞上鈉電流(INa)、鈣電流(ICa)、瞬時外嚮鉀電流(Ito)和內嚮整流鉀電流(IK1)等離子通道電流的影響.結果 在體實驗結果顯示,蛇葡萄素低、中和高劑量組大鼠實驗性室性心律失常的髮生率均低于對照組(n=5,P均＜0.05).體外全細胞膜片鉗實驗結果顯示蛇葡萄素低、中和高劑量組大鼠心室肌細胞動作電位時程(APD)均大于對照組,動作電位幅值也均低于對照組[(120.1±7.4)、(113.2±9.0)和(101.8±5.1) mV比(134.1±6.9) mY,n=9,P均＜0.05].蛇葡萄素低、中和高劑量組大鼠心室肌細胞INa峰值電流密度均小于對照組[(-31.03 ±2.61)、(-26.63±3.72)和(-17.55 ±4.43)pA/pF比(-36.75±3.60)pA/pF,n=9,P均＜0.05],但4組間最大峰值電位差異無統計學意義.蛇葡萄素高劑量組IK1峰值電流密度大于對照組[(-37.47±7.32)pA/pF比(-25.26±4.13)pA/pF,n=5,P＜0.05],而ICa和Ito4組間差異則無統計學意義.結論 蛇葡萄素具有抗大鼠心律失常的作用,其電生理機製為抑製INa、增彊IK1,進而延長APD.
목적 연구사포도소억제대서실성심률실상적작용급기전생리궤제.방법 재체실험,성년웅성Wistar대서채용조구법수궤분위생리염수대조조(대조조)、사포도소저제량(1 mg/kg)조、사포도소중제량(3 mg/kg)조화사포도소고제량(10 mg/kg)조4조.예처리후운용빙주오두감적방법유발대서심률실상,관찰사포도소대오두감유도적대서심률실상적보호작용.리체실험,사용매해법급성분리대서심실기세포,병응용막편겸기술기록사포도소대대서심실기세포상납전류(INa)、개전류(ICa)、순시외향갑전류(Ito)화내향정류갑전류(IK1)등리자통도전류적영향.결과 재체실험결과현시,사포도소저、중화고제량조대서실험성실성심률실상적발생솔균저우대조조(n=5,P균＜0.05).체외전세포막편겸실험결과현시사포도소저、중화고제량조대서심실기세포동작전위시정(APD)균대우대조조,동작전위폭치야균저우대조조[(120.1±7.4)、(113.2±9.0)화(101.8±5.1) mV비(134.1±6.9) mY,n=9,P균＜0.05].사포도소저、중화고제량조대서심실기세포INa봉치전류밀도균소우대조조[(-31.03 ±2.61)、(-26.63±3.72)화(-17.55 ±4.43)pA/pF비(-36.75±3.60)pA/pF,n=9,P균＜0.05],단4조간최대봉치전위차이무통계학의의.사포도소고제량조IK1봉치전류밀도대우대조조[(-37.47±7.32)pA/pF비(-25.26±4.13)pA/pF,n=5,P＜0.05],이ICa화Ito4조간차이칙무통계학의의.결론 사포도소구유항대서심률실상적작용,기전생리궤제위억제INa、증강IK1,진이연장APD.
Objective To explore the antiarrhythmic mechanism of ampelopsin through electrophysiological study in rats.Methods The in vivo experimental groups were as follows:control group,low-dose,middle-dose and high-dose group.Arrhythmia in rats was induced by aconitine injection,and then the antiarrhythmic effects of ampelopsin were studied.Cardiomyocytes were isolated from rats therafter.The whole-cell patch-clamp technique was used to record action potential duration (APD),sodium currents (INa),calcium current (ICa),transient outward potassium currents (Ito) and inward rectifier potassium currents (IK1) in cardiomyocytes.Results In vivo experiments showed that the incidence of aconitineinduced experimental arrhythmias in low,middle and high-dose ampelopsin group was significandy lower than that in control group (n =5 each group,all P ＜ 0.05).In vitro whole-cell patch clamp experiments showed that action potential duration in low,middle and high-dose groups was significantly shorter than that in control group,and amplitude of action potential was also significantly lower in low,middle and high-dose ampelopsin groups than in control group (134.1 ±6.9),(120.1 ±7.4),(113.2 ±9.0),and (101.8 ±5.1) mV for control,low,middle and high-dose group (n =9 each group,all P ＜ 0.05).Further research revealed that sodium currents in cardiomyocytes were decreased by low,middle and high-dose ampelopsin from (-36.75 ±3.60) to (-31.03 ±2.61),(-26.63 ±3.72),and (-17.55 ±4.43) pA/pF (n =9each group,all P ＜ 0.05),but the activation voltage for peak potential was not affected by ampelopsin.Moreover,the inward rectifier potassium current was also higher in high-dose ampelopsin group than in control group (P ＜ 0.05).Calcium current and transient outward potassium current were similar among four groups.Conclusion Ampelopsin exerts anti-arrhythmic effects in this rat model,and the underlying electrophysiological mechanism is partly associated with the inhibition of INa and enhancement of IK1,and prolongation of APD.
