论文部分内容阅读
目的:观察不同浓度外源性磷酸肌酸(phosphocreatine,PCr)对大鼠缺血心室中层心肌细胞(M细胞)瞬间外向钾通道(Ito)电流的影响,探讨其预防缺血性心律失常的电生理学机制。方法:单个M细胞经酶解从大鼠左心室中层获得,采用膜片钳全细胞模式记录Ito电流,通过灌注模拟缺血液并充以95%N2+5%CO2的混合气体建立缺血模型,将PCr加入模拟缺血液中分别配成终浓度5、10、20和30 mmol/L。将细胞分成6组,分别给予模拟缺血液,含有5、10、20和30 mmol/L PCr的模拟缺血液以及台氏液灌流,后者充以95%O2+5%CO2的混合气体。10 min后记录各组的峰电流及电流密度。结果:与台氏液组相比,单纯模拟缺血液组Ito峰电流密度降低(76.1±6.3)%(P<0.05),含有5、10、20和30 mmol/L PCr的模拟缺血液组Ito峰电流密度分别降低(57.1±9.6)%(P<0.05)、(40.3±10.3)%(P<0.05)、(34.3±9.6)%(P<0.05)和(32.1±10.6)%(P<0.05)。PCr为0、5、10 mmol/L时三者峰电流密度具有明显差异(P<0.05)。PCr为10、20、30 mmol/L对Ito峰电流密度的影响无显著差异(P>0.05)。结论:PCr能增加缺血时受抑制的M细胞Ito峰电流及电流密度,这可能是其预防缺血性心律失常的电生理学机制。低浓度(0～10 mmol/L)PCr对Ito峰电流及电流密度的影响呈现明显的量效关系。
OBJECTIVE: To observe the effects of different concentrations of exogenous phosphocreatine (PCr) on the outward Ito current in ischemic cardiomyocytes of middle cerebral artery (M) in rats, Physiological mechanisms. Methods: Single M cells were obtained from left ventricular middle layer of rats by enzymolysis. Ito current was recorded by patch clamp whole cell model. The ischemic model was established by perfusion of mixed air with simulated ischemia and filled with 95% N2 + 5% CO2. The PCr was added to simulated ischemic solution to make the final concentration of 5, 10, 20 and 30 mmol / L, respectively. The cells were divided into 6 groups, each of which was given simulated ischemia, simulated ischemic solution containing 5, 10, 20 and 30 mmol / L PCr and Tyrode’s solution perfusion, the latter being filled with 95% O2 + 5% CO2 mixed gas. After 10 min, the peak current and current density of each group were recorded. Results: Compared with Taishu liquid group, the Ito peak current densities in pure simulated ischemic group decreased significantly (76.1 ± 6.3)% (P <0.05), and those in simulated ischemic group containing 5, 10, 20 and 30 mmol / (P <0.05), (40.3 ± 10.3)% (P <0.05), (34.3 ± 9.6)% (P <0.05) and (32.1 ± 10.6)% 0.05). When the PCr was 0, 5, and 10 mmol / L, the peak current density was significantly different (P <0.05). PCr of 10,20,30 mmol / L on the Ito peak current density was no significant difference (P> 0.05). Conclusion: PCr can increase Ito peak current and current density of M cells inhibited by ischemia, which may be its electrophysiological mechanism of preventing ischemic arrhythmia. The effect of PCr at low concentration (0 ~ 10 mmol / L) on Ito peak current and current density showed a significant dose-effect relationship.