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目的：研究凝血酶诱导的血小板活化中细胞内钙动员和Ｎａ＋／Ｈ＋交换的关系．方法：Ｆｕｒａ２负载测［Ｃａ２＋］ｉ和ＢＣＥＣＦ负载测ｐＨｉ．结果：凝血酶０１ＩＵ·Ｌ－１引起［Ｃａ２＋］ｉ和ｐＨｉ增加，［Ｃａ２＋］ｉ增加先于ｐＨｉ增加．在无钠溶液中，Ｎａ＋／Ｈ＋交换被抑制而［Ｃａ２＋］ｉ增加不受影响；用尼日利亚菌素（１ｍｇ·Ｌ－１）使胞内酸化可抑制［Ｃａ２＋］ｉ增加．用依他酸（ＥＧＴＡ）阻断外钙内流，胞浆碱化不受影响．伊屋诺霉素加ＥＧＴＡ耗竭胞内钙池时，胞浆硷化效应被取消，且静息ｐＨｉ更低，加入１ｍｍｏｌ·Ｌ－１外钙重新充填钙池，胞浆碱化效应又被恢复．结论：细胞内钙动员调控Ｎａ＋／Ｈ＋交换，后者需［Ｃａ２＋］ｉ增加达一定有效浓度．
AIM: To investigate the relationship between intracellular calcium mobilization and Na + / H + exchange during thrombin-induced platelet activation. Methods: Fura 2 load measured [Ca2 +] i and BCECF load measurement pHi. RESULTS: Thrombin 0.1 IU · L-1 caused an increase in [Ca2 +] i and pHi, while [Ca2 +] i increased earlier than pHi. In sodium-free solution, Na + / H + exchange was inhibited and [Ca2 +] i increase was not affected; intracellular acidification with Nigericin (1 mg · L-1) inhibited [Ca2 +] i increase. With EGTA block external calcium influx, cytoplasmic alkalis are not affected. When ionomycin plus EGTA depleted intracellular calcium pool, the cytosolic alkaline effect was abolished, and resting pHi was lower. Adding 1 mmol·L-1 extra-calcium to recharge the calcium pool, the cytosolic alkalosis was restored . CONCLUSION: Intracellular calcium mobilization regulates Na + / H + exchange, which increases [Ca2 +] i up to a certain effective concentration.