中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2003年
21期
2918-2919
,共2页
李泱%王琳%邱萍%王士雯%姚伟星%夏国瑾%江明性
李泱%王琳%邱萍%王士雯%姚偉星%夏國瑾%江明性
리앙%왕림%구평%왕사문%요위성%하국근%강명성
动作电位%钾通道 /药物作用%蛋白激酶 C
動作電位%鉀通道 /藥物作用%蛋白激酶 C
동작전위%갑통도 /약물작용%단백격매 C
目的:研究苄基四氢帕马汀( BTHP)经蛋白激酶 C对豚鼠心肌细胞延迟整流钾电流的作用极其在临床中的应用前景. 方法:应用膜片钳在全细胞模式下记录延迟整流钾电流( Ik). 结果:PMA 10.0 μ mol/L在细胞内给药可使 Ik 和 Ik,tail增加,电流密度分别从 (13.1± 1.4) pA/pF和 (5.1± 0.7 ) pA/pF 增至 (19.5± 0.7)pA/pF和 (7.3± 0.4) pA/pF.应用 BTHP后上述增加效应被明显减少, BTHP的抑制作用在单独应用时为 (38± 6) %和 (36± 6)%,而在预先应用 PMA后 BTHP的抑制作用增加至 (64± 7) % 和 (64± 6 )%. 结论:BTHP对 Ik 和 Ik,tail的阻滞作用可能部分与抑制细胞内蛋白激酶 C途径有关.
目的:研究芐基四氫帕馬汀( BTHP)經蛋白激酶 C對豚鼠心肌細胞延遲整流鉀電流的作用極其在臨床中的應用前景. 方法:應用膜片鉗在全細胞模式下記錄延遲整流鉀電流( Ik). 結果:PMA 10.0 μ mol/L在細胞內給藥可使 Ik 和 Ik,tail增加,電流密度分彆從 (13.1± 1.4) pA/pF和 (5.1± 0.7 ) pA/pF 增至 (19.5± 0.7)pA/pF和 (7.3± 0.4) pA/pF.應用 BTHP後上述增加效應被明顯減少, BTHP的抑製作用在單獨應用時為 (38± 6) %和 (36± 6)%,而在預先應用 PMA後 BTHP的抑製作用增加至 (64± 7) % 和 (64± 6 )%. 結論:BTHP對 Ik 和 Ik,tail的阻滯作用可能部分與抑製細胞內蛋白激酶 C途徑有關.
목적:연구변기사경파마정( BTHP)경단백격매 C대돈서심기세포연지정류갑전류적작용겁기재림상중적응용전경. 방법:응용막편겸재전세포모식하기록연지정류갑전류( Ik). 결과:PMA 10.0 μ mol/L재세포내급약가사 Ik 화 Ik,tail증가,전류밀도분별종 (13.1± 1.4) pA/pF화 (5.1± 0.7 ) pA/pF 증지 (19.5± 0.7)pA/pF화 (7.3± 0.4) pA/pF.응용 BTHP후상술증가효응피명현감소, BTHP적억제작용재단독응용시위 (38± 6) %화 (36± 6)%,이재예선응용 PMA후 BTHP적억제작용증가지 (64± 7) % 화 (64± 6 )%. 결론:BTHP대 Ik 화 Ik,tail적조체작용가능부분여억제세포내단백격매 C도경유관.
AIM:To investigate influence of BTHP on the delayed rectifier potassium current by protein kinase C pathway in Guinea pig ventricular myocytes and its prospect in clinic. METHODS:Ik was recorded using whole cell arrangement of the patch-clamp procedure. RESULTS:Phorbol 12-myristate 13-acetate( PMA,10.0 μ mol/L) caused an enhance effect on Ik intercellularly, with increasing of Ik and Ik,tail from (13.1± 1.4) pA/pF and (5.1 ± 0.7 ) Pa/pF to (19.5± 0.7) pA/pF and (7.3± 0.4) pA/pF.Inhibition effect of BTHP on Ik was markedly augmented after pre-application of PMA.Inhibition rates of Ik and Ik,tail were increased from (38± 6)% and (36± 6)% only with BTHP to (64± 7)% and (64± 6)% in the exposure to BTHP together with PMA. CONCLUSION:Block of BTHP on Ik is suggested partly connecting with regulation of PKC in the guinea pig ventricular myocytes.BTHP extracted from medicinal plant origin is a new potassium channel blocker.Its potential as a frequency-dependent class Ⅲ antiarrhythmic agent is arousing great interest.