目的：探讨茶多酚对缺血/再灌注心脏损伤的保护作用，并研究心脏能量代谢和心肌细胞钙内流是否参与了心脏缺血/再灌注损伤的保护作用。方法在大鼠Langendorff离体心脏上实施缺血/再灌注各30 min，用一导管经压力换能器连接放大器记录心功能指标；用31P NMR技术测定心脏的能量代谢，全细胞膜片钳技术记录心肌细胞钙内流。结果与对照组比较，茶多酚（2.5 mg/L）能使缺血/再灌注心脏的心室发展压、左心室压最大收缩速率（+dp/dtmax）、左心室压最大舒张速率（-dp/dtmax）和冠脉流量显著增加（P<0.05），并显著改善缺血/再灌注心脏的能量代谢，增加心肌ATP和PCr含量（P<0.05）。浓度为2.5和5.0 mg/L的茶多酚均能显著抑制培养心肌细胞的钙内流（P<0.01）。结论茶多酚对大鼠离体心脏缺血/再灌注损伤的保护作用可能与其改善心肌能量代谢、抑制心肌细胞钙内流的作用有关。%Objective To investigate the protective effects of tea polyphenols (TP) against myocardial ischemia/reperfusion (IR) injuries and explore the possible mechanisms. Methods Langendorff-perfused rat hearts were subjected to ischemia for 30 min followed by reperfusion for another 30 min. Myocardial function indices were measured by a left ventricular cannula via a pressure transducer connected to the polygraph in isolated Langendorff hearts and energy metabolism was measured using 31P nuclear magnetic resonance (NMR) spectroscopy. Whole-cell patch-clamp technique was used to record calcium inward current (ICa- L) in cultured rat cardiac myocytes. Results Compared with the control hearts, the ex vivo rat hearts with 2.5 mg/L TP treatment showed significantly increased left ventricular developed pressure (LVDP), maximal rise rate of LVDP (+dp/dtmax), maximal fall rate of LVDP (-dp/dtmax), and coronary flow (CF) (P<0.05). During both cardiac ischemia and reperfusion phase, ATP and PCr levels were elevated significantly in TP-treated hearts compared with those in the control hearts (P<0.05). In cultured rat cardiac myocytes, ICa-L was remarkably decreased by TP at the doses of 2.5 and 5.0 mg/L (P<0.01). Conclusion Our results support a possible protective role of TP against myocardial IR injury by improving myocardial energy metabolism and inhibiting ICa-L in the cardiac myocytes.
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