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目的:观察急性缺血对窦房结(sino-atrial node,SAN)起搏细胞(pacemaker cells,PCs)自发性电活动的影响及肌浆网(sarcoplasmic reticulum,SR)钙释放特异性阻断剂雷诺定的干预作用,探讨SR钙释放在急性缺血诱导的心动过缓中的作用。方法:实验分为2组:非干预组(实验Ⅰ组),细胞先灌流正常台式液作为对照;记录自发性动作电位(action potential,APs)后,灌流缺血样台式液(低pH、无葡萄糖以及100%N2饱和)5~8 min模拟缺血;最后用正常台式液冲洗。雷诺定干预组(实验Ⅱ组)在灌流缺血样台式液5~8 min之前,先灌流40μmol/L雷诺定15 min,其他实验步骤同实验Ⅰ组。结果:实验Ⅰ组灌流缺血样台式液5~8 min后起搏频率(beating rate,BR)减慢13%(P<0.05),APs的超射值(overshoot,OS)增大+6 mV(P<0.01),APs时程(actionpotential duration,APD)延长44%(P<0.05),而最大舒张期电位(maxi mumdiastolic potential,MDP)无显著变化;实验Ⅱ组经雷诺定干预处理15 min后,BR减慢12%(P<0.05),灌流缺血样台氏液5~8 min后,BR进一步减慢23%(P<0.01),OS增大+5 mV(P<0.05),APD延长29%(P<0.05)。结论:5~8 min缺血可改变单个家兔SAN PCs自发性电活动,而雷诺定不能阻断该效应,提示SR钙释放可能在急性缺血诱导的家兔单个SANPCs起搏过缓中的作用不大。
Objective: To observe the effect of acute ischemia on the spontaneous electrical activity of pacemaker cells (PCs) in sino-atrial node (SAN) and the calcium-releasing specific blockers of sarcoplasmic reticulum (SR) Reynoldine intervention to explore SR calcium release in acute ischemia-induced bradycardia in the role. Methods: The experiment was divided into two groups: the non-intervention group (experimental group Ⅰ), the cells were pre-perfusion normal table fluid as a control; after recording the action potential (APs), perfusion- Glucose and 100% N2 saturation) 5 ~ 8 min simulated ischemia; and finally rinsed with normal desktop fluid. Reynoldine intervention group (experimental group II) before perfusion of ischemic sample solution 5 ~ 8 min, first perfusion 40μmol / L Reynolds 15 min, the other experimental steps with experimental group Ⅰ. Results: The beating rate (BR) decreased by 13% (P <0.05) and the overshoot (OS) of APs increased by +6 mV (P <0.01), APs prolonged by 44% (P <0.05), while maximal mmax (MDP) showed no significant change. In group Ⅱ, Renuocid intervention was used for 15 min BR decreased by 12% (P <0.05), BR decreased by 23% (P <0.01) and OS increased by +5 mV (P <0.05) The APD was prolonged by 29% (P <0.05). CONCLUSIONS: 5 ~ 8 min ischemia can change the spontaneous electrical activity of SAN PCs in a single rabbit, whileRenorodine can not block this effect, suggesting that SR calcium release may be a sign of acute bradycardia in single SANPCs not so useful.