钙通道与胎盘钙转运

钙离子的代谢和跨细胞转运在机体的多种基本生理过程中起重要作用,如神经传递、兴奋收缩耦联、囊泡分泌等.胎盘是母体胎儿间联系的纽带,胎儿需要的全部营养物质需经胎盘进行转运.胎盘滋养层细胞表达多种与钙离子转运相关的通道,如:电压依赖性通道、瞬时型受体电位通道、钙池操纵钙通道、钙结合蛋白、血浆膜和钠钙交换体等.这些通道的组织分布和功能性质各不相同.     

钙通道与胎盘钙转运

钙离子的代谢和跨细胞转运在机体的多种基本生理过程中起重要作用,如神经传递、兴奋收缩耦联、囊泡分泌等.胎盘是母体胎儿间联系的纽带,胎儿需要的全部营养物质需经胎盘进行转运.胎盘滋养层细胞表达多种与钙离子转运相关的通道,如:电压依赖性通道、瞬时型受体电位通道、钙池操纵钙通道、钙结合蛋白、血浆膜和钠钙交换体等.这些通道的组织分布和功能性质各不相同.     

无机盐类的胎盘转运

钙、磷、镁三种具有骨化作用的无机盐类均可经胎盘主动转运,而且在妊娠晚期转运速率明显增加。母体和胎儿的胎盘血流,以及母体和胎儿各自的钙浓度、1,25(OⅡ),2D_3、PTⅡ和PTⅡrP可能为钙转运的调节因素。胎盘对磷的摄取为钠依赖性的,且可因缺氧和为代谢毒物所减少;其转运可被PTⅡ而减少且受pH、温度、钠和氨基酸浓度的调节。同样,镁的转运具有温度依赖性,同时依靠钠、镁离子的交换。三种无机盐类转运的程度均具有种属差异,转运的启动机制尚不清楚。     

钙代谢与儿科危重病症

钙代谢与儿科危重病症济宁医学院附属医院儿科（２１２７２５）朱萍，王瑜综述李士玉审校钙离子对机体各种组织的功能和物质代谢的调节有着非常重要的作用。危重病症时机体出现器官功能障碍和物质代谢紊乱，钙的代谢势必也会有一定的变化，本文就儿科危重病症时钙的代谢综...     

钙通道阻滞剂对缺血再灌注兔脑皮层NO和含水量及细胞内游离钙的影响

目的　探讨一氧化氮 (NO)在缺血再灌注脑损伤中的作用 ,比较两类钙通道阻滞剂的脑保护作用。方法　采用四血管夹闭法制作兔脑缺血再灌注模型。首先测定假手术及再灌注不同时间兔脑皮层NO及含水量。并将动物分为假手术组、安慰剂组、尼莫地平组、氯胺酮组、尼莫地平 +氯胺酮治疗组 ,于再灌注 30min开始持续静脉给药至再灌注 6h。测定脑皮层NO、含水量、细胞内游离钙([Ca2 + ]i)相对荧光强度。结果　再灌注后脑皮层NO、含水量逐渐升高 ,于再灌注 6h达较高水平 [分别为 (14 7± 1 7) μmol/g ,(86 7± 1 9) % ,P <0 0 5 ],NO与含水量间具有相关性 (P <0 0 1)。尼莫地平、尼莫地平 +氯胺酮组NO明显降低 [分别为 (5 1± 0 9) μmol/g、(5 1± 1 1) μmol/g ,P <0 0 1],尼莫地平、氯胺酮以及尼莫地平 +氯胺酮组含水量明显降低 [分别为 (76 3± 4 0 ) %、(81 0± 1 9) %、(78 2± 1 4 ) % ,P <0 0 1],尼莫地平组较氯胺酮组降低更明显 (P <0 0 1)。安慰剂组 [Ca2 + ]i 较假手术组明显升高 [分别为 (2 6 8± 1 4 )、(5 0± 0 4 ) ,P <0 0 1],尼莫地平、氯胺酮及尼莫地平 +氯胺酮治疗后 [Ca2 + ]i 明显降低 [分别为 (7 7± 1 1)、(13 3± 2 0 )、(9 0± 2 0 ) ,P <0 0 1]。尼莫地平组较氯胺酮     

心脏肌浆网钙转运蛋白基因表达与调节

心肌细胞肌浆网钙转运蛋白通过调节细胞内游离钙浓度对心肌细胞的收缩,舒张功能起着决定性作用。近年来研究表明,心肌ＳＲ钙转运蛋白表达异常是多种心脏病的重要病理生理机制。目前已恨现多种参与ＳＲ钙转运蛋白表达调控的因素。     

心脏肌浆网钙转运蛋白基因表达与调节

心肌细胞肌浆网（ｓａｒｃｏｐｌａｓｍｉｃｒｅｔｉｃｕｌｕｍ，ＳＲ）钙转运蛋白通过调节细胞内游离钙浓度对心肌细胞的收缩、舒张功能起着决定性作用。近年来研究表明，心肌ＳＲ钙转运蛋白表达异常是多种心脏病的重要病理生理机制。目前已发现多种参与ＳＲ钙转运蛋白表达调控的因素。     

细胞内钙失衡在肾损伤中的作用及防治

细胞内游离钙是介导细胞生理和病理作用的重要信使，其浓度异常升高会引起细胞的急慢性损伤和死亡；同时也造成肾血液动力学改变，导致肾小球细胞增生、肥大，促进肾脏病的慢性进展。钙拮抗剂不仅降低全身血压，还抑制肾实质细胞增生、调节系膜处理大分子物，清除和减少自由基产生，降低残存肾代谢，减轻肾钙化。因此，钙拮抗剂已用于防治缺血、某些药物引发的肾损伤，延缓慢性肾功能不全的进展，减少移植肾排斥反应等。     

家兔急性缺氧后左心室舒张功能和心肌细胞内钙转运及能量代谢的研究

为探讨急性缺氧对家兔左心室舒张功能、心肌细胞内钙转运和能量代谢的影响。将２３只家兔分为对照组（６只）、吸入５％低氧混合气的缺氧１组（Ｈ１）（１２只）、吸入１０％低氧混合气的缺氧２组（Ｈ２）（５只），用心导管法测定左心室压力下降最大速率（ＬＶｄｐ／ｄｔｍａｘ）和压力下降时间常数（Ｔ值）；测定心肌肌浆网（ＳＲ）钙ＡＴＰ酶活性、心肌ＳＲ摄钙量、心肌组织ＡＴＰ和磷酸肌酸（ＣｒＰ）。结果，缺氧后ＬＶｄｐ／ｄｔｍａｘ下降，Ｔ值延长；缺氧组心肌ＳＲ钙ＡＴＰ酶活性及摄钙量下降；心肌线粒体钙含量升高；心肌组织ＡＴＰ和ＣｒＰ下降，心肌组织ＡＴＰ与线粒体钙含量呈负相关。提示，急性缺氧可引起左心室舒张功能障碍并影响心肌ＳＲ钙转运和心肌能量代谢。     

Endocrine control and disturbances of calcium and phosphate metabolism in children

Most disorders of extracellular calcium and phosphate metabolism in childhood can be attributed to primary increased or decreased secretion/action of 1,25-dihydroxyvitamin D₃ and parathyroid hormone or primary increased or decreased urinary excretion of phosphate and calcium. Based on this pathogenetic classification the most important diseases related to calcium and phosphate metabolism will be discussed.Abbreviations PTH parathyroid hormone - 1,25(OH)₂D₃ 1,25-dihydroxyvitamin D₃ - 25(OH)D₃ 25-hydroxyvitamin D₃ - 24,25(OH)₂D₃ 24,25-dihydroxyvitamin D₃ - VDR vitamin D deficiency rickets - VDDR vitamin D dependency rickets - MEN multiple endocrine neoplasia - HP hypoparathyroidism - PHP pseudohypoparathyroidism - AHO Albright's hereditary osteodystrophy - XLH X-linked familial hypophosphataemic rickets     

Fetal control of calcium transport across the rat placenta

Control of maternofetal calcium transfer across the in situ perfused rat placenta at day 21 of gestation (term 23 d) was investigated in both intact fetuses and those parathyroidectomized by decapitation on day 19. Decapitation resulted in significant fetal hypocalcemia. Injection of fetuses subcutaneously through the uterine wall with 0.43 micrograms bovine (b) PTH(1-84), 20 ng 1,25(OH)2D3 or 10 microL of the appropriate diluent resulted 2 h later in a raised fetal blood ionized Ca concentration only with bPTH(1-84) in both normal and decapitated fetuses. Fetal decapitation caused a significant (p less than 0.001) fall in the clearance of 45Ca across the placenta (Kmf45Ca), which was significantly (p less than 0.05) reversed after fetal bPTH(1-84) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) injection, but not back to normal levels. There was no effect of either hormone on Kmf45Ca in placentas from intact fetuses, or on Kmf51Cr-EDTA (used as an extracellular marker) in either group. When 4 ng/mL r[Nle8,21, Tyr34] PTH(1-34), 50 pg/mL 1,25(OH)2D3 or the appropriate diluent was perfused through placentas the only response observed was a significant (p less than 0.05) increase in Kmf45Ca with 1,25(OH)2D3 perfusion in placentas from decapitated fetuses, Kmf51Cr-EDTA being unchanged. Finally, perfusion with 10(-5) M forskolin (an activator of adenylate cyclase) stimulated Kmf45Ca in placentas from both normal and decapitated fetuses. Although there was also some effect on Kmf51Cr-EDTA in the latter, there was none in the placentas from normal fetuses, and here the effect on Kmf45Ca was dose dependent with an initial response at 10(-6) M.(ABSTRACT TRUNCATED AT 250 WORDS)     

Calcium metabolism and vitamin D metabolite levels in children receiving anticonvulsant drugs

Calcium metabolism and plasma concentrations of vitamin D metabolites were investigated in 27 children on long-term anticonvulsant therapy. Serum calcium was in the low normal range, phosphorus was normal, parathyroid hormone concentrations and alkaline phosphatase were elevated. Plasma 25-hydroxyvitamin D (25-OH D) and 24,25-dihydroxyvitamin D (24,25-(OH)₂D) were decreased, but 1,25-dihydroxyvitamin D (1,25-(OH)₂D) was normal when compared with a synchronous control group. The serum concentrations of all anticonvulsant drugs given were measured. The decreases in 25-OH D and 24,25-(OH)₂D did not depend on the blood level of a single drug, or any combination of drugs given, or on the duration of therapy. The 25-OH D levels were negatively correlated with the number of different drugs used, which may reflect the severity of the neurologic disorder, and therefore with non-specific factors such as exposure to sunlight, nutrition, or physical activity.Our data do not support the hypothesis that anticonvulsant drugs act on vitamin D metabolism.Dedicated to Prof. Dr. G.-A. von Harnack on occasion of his 65th birthday     

法洛四联症患儿心肌细胞内钙运转与心功能关系的研究

目的探讨法洛四联症(TOF)患儿心肌细胞钙运转与心功能的关系.方法钙荧光指示剂Fura-2法测定心肌细胞游离钙浓度,HP-1000型超声心动图机测定心功能.结果28例TOF患儿红细胞游离钙和总钙浓度较健康组明显高,而钙泵活性明显低下;其中8例舒张功能正常者红细胞钙泵活性与健康组无差别,而20例舒张功能异常者不仅钙泵和钠泵活性较舒张功能正常者明显下降,且红细胞游离钙和总钙浓度亦较舒张功能正常者升高.结论TOF患儿心肌细胞内钙运转与其心肌舒张功能异常密切相关.     

On the pathogenesis of anticonvulsant-drug-induced alterations of calcium metabolism

Conclusion Recent investigations have illuminated the pathogenesis of anticonvulsant-drug-induced alterations of calcium metabolism. Antiepileptic drugs may provoke renal conservation of calcium and phosphate and possibly compensate partly other of the above mentioned negative effects on calcium and bone metabolism. This may explain the relatively low incidence of manifest rickets or osteomalacia despite long-term treatment with drugs that are now well known to interfere with so many improtant factors of calcium homeostasis.Curriculum vitae. Klaus Kruse was born 1943 in Eutin, Germany. Graduation and thesis 1969 at the faculty of Medicine in Kiel, Germany. 1971 and 1972 fellowship at the Institute of Medical Molecular Biology of the Medical Academy of Lübeck, Germany. Postgraduate training in Pediatrics at the Children's Hospital of the Medical Academy Lübeck (Director: Prof. H. G. Hansen). Since 1974 clinical training at the Children's Hospital of the University of Kiel under Prof. H.-R. Wiedemann and Prof. J. Schaub. Main research interest: Pediatric endocrinology, especially disorders of calcium and carbohydrate metabolism. Member of the European Society for Pediatric Research since 1981. Recipient of a stipend from the German Research Council (studies on the pathogenesis of idiopathic hyperaclciuria and anticonvulsant bone disease).     

肺炎对幼鼠心肌线粒体钙转运及能量代谢的影响

目的 探讨肺炎对心脏功能影响的机制。方法 采用气管内接种的方法建立幼鼠金黄色葡萄球菌肺炎模型,分离心肌线粒体,观察心肌线粒体Ｃａ＾２＋－ＡＴＰ酶活性,游离钙含量,钙摄取率和释放率以及心肌组织ＡＴＰ含量,结果 与对照组相比,肺炎组心肌线粒体Ｃａ＾２＋－ＡＴＰ酶活性下降（Ｐ〈０．０５）,游离钙含量升高（Ｐ〈０．０５）,钙摄取速率下降（Ｐ〈０．０５）,钙释放速率升高（Ｐ〈０．０５）,心肌组织ＡＴＰ含量下