中国临床药理学杂志
中國臨床藥理學雜誌
중국림상약이학잡지
The Chinese Journal of Clinical Pharmacology
2015年
22期
2240-2242
,共3页
甘松新酮%快速性心律失常%心肌细胞%抑制%机制
甘鬆新酮%快速性心律失常%心肌細胞%抑製%機製
감송신동%쾌속성심률실상%심기세포%억제%궤제
nardosinone%tachyarrhythmia%myocardial cell%inhibition%mechanism
目的 研究甘松新酮对快速性心律失常大鼠心肌细胞的抑制作用. 方法用数字表法将60只健康成年雄性Wistar大鼠随机分为正常组、模型组及甘松新酮组,各20 只. 模型组、甘松新酮组大鼠舌下静脉注射0.002%乌头碱1 mL·kg-1 ,建立快速性心律失常动物模型. 甘松新酮组大鼠腹腔注射甘松新酮100 μg·g-1 (约0.5 mL);正常组、模型组大鼠腹腔注射等量生理盐水. 用多导电生理记录仪测量各组大鼠的心率、血流动力学及心系数指标,用激光共聚焦显微镜测量心肌细胞钙离子,放免法、凝胶成像法检测环磷酸腺苷( cAMP)及蛋白激酶A( PKA)变化.结果 正常组,心率、左心室终末舒张压( LVEDP)、心系数及 Ca2+水平显著低于模型组( P <0.05 ) ,其左心室收缩压( LVSP )、+dp/dtmax、-dp/dtmax均显著高于模型组(P<0.05);甘松新酮组,上述指标较模型组有明显改善( P<0.05).正常组,心肌组织cAMP、PKA水平显著低于模型组(P<0.05);正常组与甘松新酮组的依赖蛋白激酶(cAMP)、激酶A(PKA)水平无明显差异( P>0.05). 结论 甘松新酮可通过影响cAMP-PKA细胞信号转导通路,促进心功能的恢复,抑制心肌细胞钙超载,能够明显改善快速性心律失常大鼠心律.
目的 研究甘鬆新酮對快速性心律失常大鼠心肌細胞的抑製作用. 方法用數字錶法將60隻健康成年雄性Wistar大鼠隨機分為正常組、模型組及甘鬆新酮組,各20 隻. 模型組、甘鬆新酮組大鼠舌下靜脈註射0.002%烏頭堿1 mL·kg-1 ,建立快速性心律失常動物模型. 甘鬆新酮組大鼠腹腔註射甘鬆新酮100 μg·g-1 (約0.5 mL);正常組、模型組大鼠腹腔註射等量生理鹽水. 用多導電生理記錄儀測量各組大鼠的心率、血流動力學及心繫數指標,用激光共聚焦顯微鏡測量心肌細胞鈣離子,放免法、凝膠成像法檢測環燐痠腺苷( cAMP)及蛋白激酶A( PKA)變化.結果 正常組,心率、左心室終末舒張壓( LVEDP)、心繫數及 Ca2+水平顯著低于模型組( P <0.05 ) ,其左心室收縮壓( LVSP )、+dp/dtmax、-dp/dtmax均顯著高于模型組(P<0.05);甘鬆新酮組,上述指標較模型組有明顯改善( P<0.05).正常組,心肌組織cAMP、PKA水平顯著低于模型組(P<0.05);正常組與甘鬆新酮組的依賴蛋白激酶(cAMP)、激酶A(PKA)水平無明顯差異( P>0.05). 結論 甘鬆新酮可通過影響cAMP-PKA細胞信號轉導通路,促進心功能的恢複,抑製心肌細胞鈣超載,能夠明顯改善快速性心律失常大鼠心律.
목적 연구감송신동대쾌속성심률실상대서심기세포적억제작용. 방법용수자표법장60지건강성년웅성Wistar대서수궤분위정상조、모형조급감송신동조,각20 지. 모형조、감송신동조대서설하정맥주사0.002%오두감1 mL·kg-1 ,건립쾌속성심률실상동물모형. 감송신동조대서복강주사감송신동100 μg·g-1 (약0.5 mL);정상조、모형조대서복강주사등량생리염수. 용다도전생리기록의측량각조대서적심솔、혈류동역학급심계수지표,용격광공취초현미경측량심기세포개리자,방면법、응효성상법검측배린산선감( cAMP)급단백격매A( PKA)변화.결과 정상조,심솔、좌심실종말서장압( LVEDP)、심계수급 Ca2+수평현저저우모형조( P <0.05 ) ,기좌심실수축압( LVSP )、+dp/dtmax、-dp/dtmax균현저고우모형조(P<0.05);감송신동조,상술지표교모형조유명현개선( P<0.05).정상조,심기조직cAMP、PKA수평현저저우모형조(P<0.05);정상조여감송신동조적의뢰단백격매(cAMP)、격매A(PKA)수평무명현차이( P>0.05). 결론 감송신동가통과영향cAMP-PKA세포신호전도통로,촉진심공능적회복,억제심기세포개초재,능구명현개선쾌속성심률실상대서심률.
Objective To investigate the inhibitory effect of nardosinone on myocardial cell in rats with tachyarrhythmia.Methods A total of 60 healthy adult male Wistar rats were randomly divided into normal group, model group and nardosinone group with 20 rats in each one. The 0.002%aconitine 1 mL·kg -1 was used to treat rats in model group and nardosinone group. After the establishment of tachyarrhythmia animal model, 100 μg·g -1(about 0.5 mL) nardosinone was used to treat rats in nardosinone group by intraperitoneal injection.Heart rate, hemody-namics and heart coefficient index were measured using multi-conduc-tive physiological recorder.Calcium ion ( Ca2+) in myocardial cell was measured using laser confocal microscope.Cyclic adenosine monophos-phate ( cAMP ) and protein kinase A ( PKA ) changes were detected using radioimmunoassay and gel imaging.Results In the normal group, heart rate, left ventricular end -diastolic pressure ( LVEDP ) , heart coefficient, Ca2+ level were significantly lower than those of model group.And the left ventricular systolic pressure(LVSP), +dp/dtmax,-dp/dtmax were significantly higher than those in of model group (P<0.05).Compared with the model group, the a-bove indicators have been improved in nardosinone group(P<0.05).In the normal group, myocardial cyclic adeno-sine monophosphate(cAMP), PKA level was significantly lower than those of model group (P<0.05).Difference of cAMP and PKA between normal group and nardosinone group was not significant (P>0.05).Conclusion Nardosi-none can affect the signal transduction pathway of cAMP-PKA cells, promote the recovery of cardiac function and in-hibit calcium overload in myocardial cells, thus significantly improving the heart rate in rats with cardiac arrhythmia.
