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中文摘要：
目的观察血小板激活因子（PAF）是否影响心室肌细胞钙离子浓度（[Ca^2＋]：）以及通过哪条信号转导通路起作用。方法采用酶法分离豚鼠心室肌细胞，用PAF刺激细胞；用Fluo-3／AM和共聚焦显微镜观察细胞[Ca^2＋]i；用2-氨乙基硼酸二苯酯（2-APB）和雷诺定（ryanodine）分别阻断IP3和雷诺定信号通路。全细胞膜片钳技术观察心室肌细胞L型钙电流（LCa-L）。结果无论在有钙还是无钙台氏液，PAF（1pmol·L^-1～10nmol·L^-1）都能增加心肌细胞[Ca^2＋]i，其作用能够被2-APB2μmol·L^-1阻断，而不能被雷诺定200μmol·L^-1阻断。PAF1nmol·L^-1对ICa-L没有明显影响，对照组和实验组电流密度分别为-（11．0±1．9）和-（10．5±1．3）pA·pF^-1。结论PAF能增加豚鼠心室肌细胞[Ca^2＋]i，IP3信号通路可能参与了这一过程。
英文摘要：
AIM To observe whether platelet activating factor （PAF） will influence cytosolic calcium concentration （ [ Ca^2 ＋ ]i） in ventricular myocytes and which signaling pathway is involoved. METHODS Ventricular myocytes were isolated enzymatically. Cells were stimulated with PAF, and [ Ca^2＋ ]i was measured with calcium indicator Fluo-3/AM and a confocal laser microscope. For the observation of signaling channel mediated by inositol 1,4,5-trisphosphate （IP3 ） and ryanodine, 2-aminoethyl diphenylborate （ 2-APB, 2 μmol· L^ - 1 ） and ryanodine （200 μmol· L^- 1 ） were used respectively for blocking the signaling channel. Whole-cell patch clamp was used to study the effect of PAF on L-type calcium channel （ICa-L）. RESULTS PAF （1 pmol·L^-1 - 10 nmol·L^-1 ） increased [Ca^2＋ ]i in Tyrode＇s solution with or without calcium, and the APB, but not by effect was inhibited by 2- ryanodine. ICa-L was not changed by PAF 1 nmol· L^ -1 [- （ 11.0 ± 1.9 ） vs - （10.5 ±1.3） pA·pF ^-1]. CONCLUSION Increasing [ Ca^2＋ ]i of cardiomyocytes induced by PAF is associated with IP3 pathway, but has nothing to do with ICa-L and ryanodine pathway.
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