摘要
目的 :研究急性心肌梗死 (AMI)后心室肌细胞钙离子通道电流的变化。方法 :采用结扎兔冠状动脉左前降支的方法建立 AMI动物模型 ,应用膜片钳全细胞记录方法 ,观察 AMI后 1周及 2月心外膜梗死区心肌细胞 L -钙通道电流 (ICa- L)的变化。结果 :1梗死后 1周组、2月组与对照组相比 ,I- V曲线上移。ICa- L电流密度峰值 (0 m V时 )的比较显示 :对照组为 5 .6± 1.5 p A/ pf(n=10 ) ;梗死后 1周组为 3.5± 0 .9p A / pf(n=6 ) ,较对照组显著减小 ,P<0 .0 5 ;梗死后 2月组为 4 .8± 1.5 p A/ pf(n=11) ,较对照组减小 ,较梗死后 1周组增大 ,但均无统计学差异 ,P>0 .0 5。 2梗死后 1周组、梗死后 2月组与对照组相比 ,失活曲线明显左移 (即向超极化方向移动 ) ,以梗死后 1周组左移更加明显。梗死后 1周组半数失活电压 (V0 .5)为 - 2 6± 7m V(n=6 ) ,与对照组 (- 13± 4 m V ,n=8)比较相差显著 ,P<0 .0 5。梗死后 2月组半数失活电压 V0 .5为 - 2 1± 6 m V(n=8) ,与对照组比较无统计学差异 ,P>0 .0 5。结论 :AMI后1周梗死区心室肌细胞 ICa- L下降、钙通道动力学发生变化 ,在 AMI后
AIM:To study the current density and function of L calcium channel in cells from the epicardial border zone of the 1 week and 2 month infarcted rabbit hearts. METHODS:Rabbits were infarcted by ligation of the left anterior descending coronary artery,1 week(PMI 1 wk) and 2 month(PMI 2 mo) later, I Ca L was recorded using whole cell patch clamp techniques from infarcted heart and compared with the I Ca L from the noninfarcted heart(Con). RESULTS:Peak I Ca L current density(at 0 mV) was significantly reduced in PMI 1 wk (3.5±0.9 pA/pF, n =6)compared with Con group (5.6±1.5 pA/pF, n =10), P <0.01. However, 2 month after the occlusion,the peak I Ca L density in PMI 2 mo(4.8±1.5 pA/pF, n =11) was not significantly different from that of the Con group, although there was slight reduction in it . V 0.5 of the availability curve was shifted significantly in the hyperpolarizing direction in PMI 1 wk (-26±7 mV, n =6) compared with that of the Con group (-13±4 mV, n =8), P <0.05. V 0.5 was also shifted in the hyperpolarizing direction in PMI 2 mo(-21±6 mV, n =8) compared with that of the Con group,although this shift was not significant, P >0.05. CONCLUSION: I Ca L was reduced,and its kinetics was altered in myocytes of the infarcted zone. 2 month after the occlusion,the depressed I Ca L returned to nearly normal, suggesting the presence of reverse remodeling.
出处
《心脏杂志》
CAS
2003年第2期109-112,共4页
Chinese Heart Journal