肌浆网Ca~(2+)-ATP酶和L型-Ca~(2+)通道功能变化对肥厚心室肌电重构的影响

为探讨肌浆网Ca2 + ATP酶和L型 Ca2 +通道功能变化在左室肥厚 (LVH)心室肌电重构发生中的作用。将 60只日本大耳白兔随机分为 6组 :单纯实验组、实验组 +维拉帕米、实验组 +Thapsigargin、单纯对照组、对照组 +维拉帕米和对照组 +Thapsigargin。实验组行腹主动脉部分结扎术 ,喂养 1 0周制作LVH模型。对照组在游离出腹主动脉后 ,不予结扎。均采用以Langendorff离体灌流方法。对单纯实验组和单纯对照组 ,在心外膜左室心尖部部位以 2 31ms为基础周长 (BCL)测定心室有效不应期 (VERP)后 ,于右房行电刺激 ,刺激频率为 2 60次 /分 ,持续 30min ,保持 1 1房室传导。刺激结束后 ,重复测定VERP值。对其余 4组 ,先测定未加药物时各组的VERP值 ,随后改用加入药物的灌流液后再次测定VERP值 ,最后进行右房刺激及VERP的测定 (同前 )。结果 :单纯实验组在快速刺激后 ,VERP显著延长 ,其延长程度显著大于单纯对照组 ;而在加用维拉帕米的实验组和对照组中 ,快速刺激后无VERP延长的表现 ;相反 ,Thapsigargin则可增强快速刺激后VERP延长的表现。结论 :L 型Ca2 +通道的激活可能是LVH心室肌电重构发生的重要原因。其中 ,心室肌细胞肌浆网Ca2 + ATP酶的功能降低参与了此过程 ,并可能导致了LVH与正常心室肌的频率相关性电重构?

The Ventricular Electrical Remodeling in Left Ventricular Hypertrophy,What Role of Sarcoplasmic Reticulum Ca~(2+)-ATPase and Ca~(2+)Channel Play in It?

To observe what role of the ca 2+ channel and the sarcoplasmic reticulum ca 2+ ATPase(SERCA2a) play in the ventricular electrical remodeling in rabbit left ventricular hypertrophy( LVH) models. The rabbits were divided into 6 groups(LVH pure , Control pure , LVH verapamil , Control verapamil , LVH thapsigargin , Control thapsigargin ). In the pure LVH and control groups, the ventricular effective refractory period(VERP) was measured(S 1S 1 =231 ms)at left ventricular apex(LVA) on the epicardium. Then the right atrium was paced at a rate of 260 ppm with 11 AV conduction for 30 minutes. After pacing, the VERP were measured as before. In the other four groups, after the first time of VERP recording, the verapamil or thapsigargin was added into the perfusate, 15 minutes later the VERP was measured for another time, and then the rabbits were subjected to right atrium pacing (260 ppm) for 30 minutes, after that, the VERP was measured for the final time. Results: The VERP in the pure LVH and control groups were increased after rapid pacing. In the two verapamil used groups, no increase of VERP was observed. On the contrary, thapsigargin can intensify the electrical remodeling, namely, increase the prolongation of VERP during rapid pacing . Conclusions: The manifestation of electrical remodeling due to rate is more significant in LVH than in the normal. The activation of L type Ca 2+ channels and the Ca 2+ overload may be the cause of electrical remodeling. The inactivation of SERCA2a may also contribute to it, and lead to the different manifestation of electrical remodeling between LVH and the normal.