目的：研究宫内急性缺血缺氧后(HI)胎鼠肾脏钙离子腺苷三磷酸酶(Ca2+-ATPase)的动态变化，探索围产期窒息后肾损伤发生细胞内钙超载的机制。方法：通过钳夹孕21 d大鼠供应子宫的动静脉血管，制成胎鼠宫内不同程度HI模型和HI后再灌注不同时间模型。采用化学方法测定胎鼠肾脏细胞膜和线粒体Ca2+-ATPase的活性变化。结果：假手术组胎肾细胞膜和线粒体Ca2+-ATPase活性分别为(7.476±0.353)和(3.470±0.270) 微摩尔磷/毫克蛋白·小时(μmol.Pi/mgprot.h)，宫内HI 15 min后Ca2+-ATPase活性均明显减弱，分别为(6.411±0.210)和(2.886±0.245) μmol.Pi/mgprot.h，(P<0.01)；与缺血15 min时比较，宫内缺血45 min时酶活性减弱更明显，分别为(5.772±0.177)和(2.500±0.282) μmol.Pi/mgprot.h，(P<0.05)。缺血15 min再灌注过程中，细胞膜和线粒体Ca2+-ATPase活性与缺血时比较继续减弱，8 h时最低，分别为(5.513±0.197)和(2.411±0.197) μmol.Pi/mgprot.h，(P<0.01)，15 h时均明显回升，至24 h时细胞膜Ca2+-ATPase活性已接近假手术组(P>0.05)，但线粒体Ca2+-ATPase活性(3.234±0.143) μmol.Pi/mgprot.h，仍低于假手术组(P<0.05)。结论：宫内HI后胎肾Ca2+-ATPase活性的降低是发生细胞内钙超载导致肾损伤的重要机制。

OBJECTIVE: To study the dynamic changes in renal Ca2+ ATPase after acute intrauterine ischemia in fetal rats,and to explore the underlying mechanism of intracelluar Ca2+ overload secondary to perinatal asphyxia.METHODS: A rat model of acute intrauterine ischemia was developed using different degrees of clamping of the vesseles supplying blood to the uterus. A graded reperfusion model was made by reperfusing the uterine vessels for different lengths of time after clamping. The activity of Ca2+ATPase in cell membranes and mitochondrial fractions in fetal rat kidneys was assayed biochemically.RESULTS: Ca2+ATPase activity in cell membranes and mitochondria in the shamoperated group was (7.476±0.353) and (3.470±0.270) μmol.Pi/mgprot.h respectively. Activities in both fractions decreased after 15 minutes of ischemia ［(6.411±0.210) and (2.886±0.245) μmol.Pi/mgprot.h respectively; P<0.01］ and continued to decrease after 45 minutes ［(5.772±0.177) and (2.500±0.282) μmol.Pi/mgprot.h respectively; P<0.05］. During the reperfusion stage (after 15 minutes of ischemia), activities continued to decrease reaching a nadir after 8 hours ［(5.513±0.197) and (2.411±0.197) μmol.Pi/mgprot.h respectively］. There was significant difference between the 8hour reperfusion group and the 15-minute ischemia group (P<0.01). After 15 h of reperfusion enzyme activity levels began to increase. By 24 hours, the activity of Ca2+ATPase in cell membranes had increased to normal levels, but the actvity in mitochondria was still low compared with the 15-minute ischemia group ［(3.234±0.143) and (2.886±0.245) μmol.Pi/mgprot.h respectively; P<0.05］. CONCLUSIONS: Ca2+ATPase activity decreases in the fetal kidney after acute intrauterine ischemia. Dynamic changes in Ca2+ATPase activity may explain the intracellular Ca2+ overload leading to hypoxic ischemic renal injury.