用酶解法分离单个豚鼠心室肌细胞，以荧光探针Ｆｌｕｏ－３／ＡＭ标记胞浆内游离钙离子，用激光扫描共聚焦显微镜实时测定胞浆内［Ｃａ２＋］ｉ变化。分别观察了在正常台氏液和无钙台氏液中３０ｍｍｏｌ／ＬＫＣｌ除极对胞浆内［Ｃａ２＋］ｉ的影响。结果表明，在正常台氏液中，３０ｍｍｏｌ／ＬＫＣｌ除极可引起胞浆内［Ｃａ２＋］ｉ持续升高，持续时间超过２５０ｓ；在无钙台氏液中，３０ｍｍｏｌ／ＬＫＣｌ除极可引起胞浆内［Ｃａ２＋］ｉ短暂升高，持续时间约１００ｓ。由此可见，在豚鼠心室肌细胞上，ＫＣｌ除极可引起胞内钙贮库的钙释放，而且这种钙释放不需要钙内流的介导。胞浆内［Ｃａ２＋］ｉ的持续性升高需要外钙内流来维持。 Single guinea pig ventricular myocytes were isolated by enzymatic digestion. Fluorescence probe Fluo-3 / AM was used to label the intracellular Ca2 +. The change of [Ca2 +] i in the cytoplasm was measured by laser confocal microscopy. The effects of 30mmol / L KCl depolarization on [Ca2 +] i in the cytoplasm of normal and non-calcium Tyrosine solution were observed respectively. The results showed that in normal Tyrode’s solution, 30mmol / L KCl depolarization could cause [Ca2 +] i in the cytoplasm to persistently increase for more than 250s; in 30mmol / L KCl decellularization, Within the [Ca2 +] i transient increase, duration of about 100s. Thus, in guinea pig ventricular myocytes, KCl depolarization can cause calcium release from intracellular calcium stores, and this calcium release is not mediated by calcium influx. The persistent elevation of [Ca2 +] i in the cytoplasm requires external calcium influx to maintain.