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目的研究粉防己碱(Tet)对大鼠缺血再灌注心脏的左室发展压、左室顺应性和对二氢吡啶拮抗剂(+)[3H]伊拉地平结合位点的影响.以硝苯地平(Nif)作为已知药对照.方法建立离体大鼠心脏缺血(30 min)再灌注(15 min)模型.大鼠预先ip Tet 30 mg*kg-1, 每日2次,连续3 d,然后离体心脏给予Tet 0.18 mmol*L-1灌流, 缺血前灌流5 min,缺血后再灌流15 min.通过连接于压力传感器的乳胶气囊测定左室发展压(LVDP)和左室顺应性;放射配基结合法测定心脏细胞膜上的(+)[3H]伊拉地平结合位点.结果与正常对照组相比,缺血再灌注使LVDP降低(42±6)%, 而经Tet处理的心脏只降低(8.6±0.2)%;缺血再灌注后左室顺应性显著受损, 左室舒张末压-容积曲线左移,Tet处理的心脏顺应性改变很小, 接近正常组.Scatchard作图分析, 正常组大鼠心脏细胞膜与(+)[3H]伊拉地平有高度结合位点,KD 为(0.16±0.03)nmol*L-1,Bmax为(0.93±0.30)nmol*g-1蛋白, 缺血再灌组心脏结合位点的密度减少[Bmax为(0.48±0.14)nmol*g-1蛋白], Tet组的Bmax较缺血再灌组明显升高[(0.68±0.12)nmol*g-1蛋白].各组的KD值均无明显差别.结论 Tet与Nif相似, 保护离体大鼠心脏的收缩功能和左室顺应性, 减轻缺血所致的二氢吡啶结合位点密度降低.这些效应伴随能量需求的下降因而阻止胞内钙超载, 改善缺血.“,”AIM To investigate if tetrandrine(Tet) modifies the affinity(KD), density(Bmax) of cardiac dihydropyridine binding sites, left ventricular(LV) compliance and LV contractile force in rat hearts with ischemia-reperfusion(I-R) injury. METHODS I-R model was built by step perfusion to make global ischemia for 30 min and then reperfusing for 15 min. Tet 30 mg*kg-1 was administrated ip, twice daily for 3 d before ischemia, and then Tet 0.18 mmol*L-1 in K-H buffer was perfused for 5 min before ischemia and for 15 min after ischemia. Left ventricular developed pressure(LVDP), LV compliance were measured with a latex balloon connected to a pressure transducer to place in the LV through the apex of the hearts. The specific binding sites of dihydropyridine antagonist isradipine on membrane of hearts were determined by radioligand binding assay. RESULTS After I-R, the LVDP reduced (42±6)%, whereas Tet-treated hearts suffered only slight declines [(8.6±0.2)%]. I-R incurred significantly LV compliance loss and caused a leftward shift of the left ventricular end diastolic pressure-volume curves, whereas Tet-treated groups displayed a minor compliance changes. Scatchard analysis indicated that a high affinity site in normal rats with KD (0.16±0.03)nmol*L-1 and Bmax (0.93±0.30)nmol*g-1 protein, I-R and Tet groups with Bmax (0.48±0.14), (0.68±0.12)nmol*g-1 protein (Tet vs I-R group, P<0.01), and without any change in KD values. CONCLUSION Like Nif, Tet protected I-R injured rat hearts from losses of mechanical function, LV compliance and reduction in density of dihydropyridine binding sites. These beneficial effects were companied by lower energy demands and prevention of cellular Ca2+ overload.