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机构地区:[1]广东省人民医院新生儿科,广州510080 [2]广东省人民医院血液流变学室,广州510080
出 处:《中华围产医学杂志》2001年第3期159-162,共4页Chinese Journal of Perinatal Medicine
基 金:2 0 0 0年广东省重点科技项目 ( 2 KM0 560 4S)
摘 要:目的 探讨地塞米松产前干预是否对宫内窘迫胎鼠脑损害有保护作用 ,以寻找围产期脑损害早期治疗的新途径。 方法 将 57只胎龄为 2 0 d的 SD大鼠的胎鼠随机分为 5组 ,即假手术组 (对照组 ,C组 ) 1 1只 ;宫内窘迫模型作为窘迫对照组 ( E组 ) 1 0只 ;宫内窘迫模型并在钳夹血管前、钳夹同时以及再灌注同时对母鼠静脉注射地塞米松 ( 1 mg/ kg)者分别为治疗 I组 ( D1组 ) 1 5只 , 组( D2 组 ) 1 2只和 组 ( D3 组 ) 9只。在再灌注 3 0 min后取脑检测各组胎鼠脑细胞内外钙、钠、钾含量。 结果 ( 1 ) E、D1、D2 和 D3 组胎鼠脑细胞内游离钙离子浓度分别为 ( 552± 94 )、( 43 8± 1 0 5)、( 44 5± 57)和 ( 456± 1 1 0 ) nmol/ L,均明显高于对照组 ( 3 1 5± 87) nmol/ L ( P<0 .0 1 )。 ( 2 ) D1组、D2 组、D3 组对母鼠注射地塞米松 ,其胎鼠脑细胞内游离钙离子浓度仍高于 C组 ,但亦均明显低于 E组 ( P<0 .0 1或0 .0 5)。( 3 ) D3 组脑组织总钠含量 ( 485± 1 85) mmol/ kg干脑 ,明显低于 E组 ( 64 1± 1 55) mmol/ kg干脑 ( P<0 .0 5)。 结论 应用地塞米松后 ,胎鼠脑细胞钙、钠超载明显减轻 ,提示产前注射地塞米松可能对胎鼠宫内窘迫脑损害有一定的保护作用。Objective To investigate whether antenatal administration of dexamethasone would provide protection against cerebral hypoxic ischemic damage in asphyxiated fetal rats. Methods Fifty seven fetal rats of twenty day gestational age were randomly divided into five groups: sham operation (normal control, n =11), asphyxiated control (group E, n =10), and group D 1?D 2?D 3 of different timings of intravenous dexamethasone treatment (1 mg/kg) in pregnant SD rats ( n =15, 12, and 9 respectively). The times assigned for dexamethasone injection were thirty minutes before clamping, the time aroung clamping and the beginning of reperfusion respectively. Intra and extra cellular concentrations of calcium, sodium and potassium in fetal rat brains were measured in each group after thirty minutes of reperfusion. Results (1)Intracellular free calcium concentrations of fetal rat brains in group E,D 1, D 2 and D 3 were 552±94, 438±105, 445±57, and 456±110 nmol/L respectively, and all significantly higher than that in the normal control 315±87 nmol/L ( P <0.01), bat significantly lower than that in the asphyxiated control (group E) ( P <0.01 or 0.05); (2) Total sodium concentrations in group D 3 (485±185 mmol/kg dry brain)were significantly lower than that in the asphyxiated control (641±155 mmol/kg dry brain)( P <0.05). Conclusion Cerebral calcium and/or sodium overloads became ameliorated after dexamethasone administration, indicating that antenatal dexamethasone therapy might provide protection against cerebral hypoxic ischemic damage for asphyxiated rat etuses.
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