龙牙楤木总皂苷对缺血/再灌注心肌细胞收缩功能和钙瞬变的影响

Effect of aralosides to contraction function and calcium transient of ischemia / reperfusion myocardial cells

为探讨龙牙楤木总皂苷(AS)对缺血/再灌注(I/R)诱导大鼠心肌细胞损伤的保护作用,采用乳酸钠灌注液灌注成年大鼠的心室肌细胞模拟缺血,含钙台式液模拟再灌注,细胞收缩与离子浓度同步测定系统同步检测AS对单个I/R细胞收缩和钙瞬变的影响。发现AS使再灌注后心肌细胞静息态肌小节长度、收缩幅度、收缩/舒张速度以及钙瞬变幅度、速度增大(P<0.05,P<0.01),细胞达到舒张时最大长度的90.0%的时间、细胞收缩达峰值的时间、稳态钙静息值、收缩期[Ca2+]i上升到最高的50.0%的时间、胞内钙瞬变衰减率减少(P<0.05,P<0.01)。因此,推测AS改善了缺血再灌注后细胞收缩与钙稳态的损伤。

To discuss the protective effect of aralosides （AS） on I/R-induced rat myocardial injury. The adult rat ventricular myocyte ischemia model was established through perfusion with sodium lactate perfusate and reperfusion with Ca^2＋ -containing Tyrode＇s solution simulation. The cell contraction and ion concentration synchronization determination system was applied to detect the effect of AS on single I/R cell contraction and Ca^2＋ transients. According to the findings, AS could increase resting sarcomcre length, contraction amplitude, ± dL/dtmax, calcium transient amplitude and speed of post-reperfusion myocardial cells （P 〈 0. 05, P 〈 0. 01 ）, and decrease in time for achieving 90. 0% of maximum relaxation, time for achieving peak value, resting calcium ratio, contraction period [ Ca^2 ＋ ] i, time for achieving 50. 0% of maximum relaxation and attenuation rate of intracellular calcium transient （ P 〈 0. 05, P 〈 0. 01 ）. Therefore, it is suggested that AS improved the post-repeffusion cell contraction and injury of calcium homeostasis.