中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2009年
2期
180-184
,共5页
刘承云%陈桂青%耿小晶%陈心%万晶晶
劉承雲%陳桂青%耿小晶%陳心%萬晶晶
류승운%진계청%경소정%진심%만정정
花生四烯酸%心室肌细胞%心律失常%L-型钙通道%膜片钳
花生四烯痠%心室肌細胞%心律失常%L-型鈣通道%膜片鉗
화생사희산%심실기세포%심률실상%L-형개통도%막편겸
Arachidonic acid%Ventricular myocytes%Arrhythmia%L-type calcium channel%Patch clamp
目的 研究花生四烯酸(arachidonic acid,AA)对家兔单个心室肌细胞L-广型钙通道的作用及其抗心律失常作用的机制.方法 采用酶解法分离得到家兔单个心室肌细胞,全细胞膜片钳技术记录单个心室肌细胞L-型钙电流(L-type calcium current,Ica-L),用累积给药的方法在灌流液中加入不同浓度的AA,观察给药前后L-型钙电流的变化,统计学方法采用单因素方差分析.结果 不同浓度的从均能明显抑制心室肌细胞,Ica-L.3 μmol/L,μmol/L,20,μmol/L的AA使Ica-L峰电流密度从(10.79±0.93)pA/pF分别减少剑(8.99 ±0.43)pA/pF、(7.60 ±0.35)pA/pF和(5.60±0.30)pA/pF(n=7,P<0.05),经冲洗后Ica-L可部分恢复,并且AA可使Ica-L的I-V关系曲线上移,其形状和峰值电压保持不变;20 μmol/L的AA使Ica-L失活曲线左移,失活后恢复时间明显延长,但对激活曲线无明显影响.结论 花生四烯酸可通过加快L-型钙通道失活,延长其失活后的恢复过程而减少细胞外钙离子的内流,延长有效不应期,从而发挥抗心律失常作用.
目的 研究花生四烯痠(arachidonic acid,AA)對傢兔單箇心室肌細胞L-廣型鈣通道的作用及其抗心律失常作用的機製.方法 採用酶解法分離得到傢兔單箇心室肌細胞,全細胞膜片鉗技術記錄單箇心室肌細胞L-型鈣電流(L-type calcium current,Ica-L),用纍積給藥的方法在灌流液中加入不同濃度的AA,觀察給藥前後L-型鈣電流的變化,統計學方法採用單因素方差分析.結果 不同濃度的從均能明顯抑製心室肌細胞,Ica-L.3 μmol/L,μmol/L,20,μmol/L的AA使Ica-L峰電流密度從(10.79±0.93)pA/pF分彆減少劍(8.99 ±0.43)pA/pF、(7.60 ±0.35)pA/pF和(5.60±0.30)pA/pF(n=7,P<0.05),經遲洗後Ica-L可部分恢複,併且AA可使Ica-L的I-V關繫麯線上移,其形狀和峰值電壓保持不變;20 μmol/L的AA使Ica-L失活麯線左移,失活後恢複時間明顯延長,但對激活麯線無明顯影響.結論 花生四烯痠可通過加快L-型鈣通道失活,延長其失活後的恢複過程而減少細胞外鈣離子的內流,延長有效不應期,從而髮揮抗心律失常作用.
목적 연구화생사희산(arachidonic acid,AA)대가토단개심실기세포L-엄형개통도적작용급기항심률실상작용적궤제.방법 채용매해법분리득도가토단개심실기세포,전세포막편겸기술기록단개심실기세포L-형개전류(L-type calcium current,Ica-L),용루적급약적방법재관류액중가입불동농도적AA,관찰급약전후L-형개전류적변화,통계학방법채용단인소방차분석.결과 불동농도적종균능명현억제심실기세포,Ica-L.3 μmol/L,μmol/L,20,μmol/L적AA사Ica-L봉전류밀도종(10.79±0.93)pA/pF분별감소검(8.99 ±0.43)pA/pF、(7.60 ±0.35)pA/pF화(5.60±0.30)pA/pF(n=7,P<0.05),경충세후Ica-L가부분회복,병차AA가사Ica-L적I-V관계곡선상이,기형상화봉치전압보지불변;20 μmol/L적AA사Ica-L실활곡선좌이,실활후회복시간명현연장,단대격활곡선무명현영향.결론 화생사희산가통과가쾌L-형개통도실활,연장기실활후적회복과정이감소세포외개리자적내류,연장유효불응기,종이발휘항심률실상작용.
Objective To study the influence of arachidonic acid (AA) on L-type calcium channel in rabbits sin-gle cardiomyocyte and its mechanism of antiarrhythmia. Method The single ventricular cardiomyocyte was isolat-ed by using enzyme dispersion method and whole-cell clamp-patch technique was used to record L-type calcium current.All data were analyzed using ANOVA. Results AA inhibited Ica-L in a concentration-dependent manner. The application of 3 μmol/L, 10 μmol/L and 20 μmol/L arachidonic acid reduced the density of peak Ica-L from (10.79±0.93)pA/pF to (8.99±0.43)pA/pF to (7.60±0.35)pA/pF and to (5.60±0.30)pA/pF, respctive-ly (n=7, P<0. O1 ). The Ica-Lpartially resumed after washout. The AA up-shifted the I-V curves of Ica-L without changes of their shape,peak and reverse potentials. The AA also markedly shifted the inactivation curve to left, and prolonged the recorvery time from inactivation,but did not change the curve of calcium channel activation. Con-clustions By acceleration of L-type calcium channel inactivation and prolongation of recorvery time from inactiva-fion,arachidonic acid can reduce the calcium ion influe and prolong effective refractory period, playing the role of antiarrhythmia.