牛磺酸对大鼠培养心肌细胞感染病毒后钙离子内流的影响

观察牛磺酸对心肌细胞感染 ＣｏｘｓａｃｋｉｅＢ３病毒（ＣＶＢ３）后 Ｃａ２＋内流的影响。取新生 ＳＤ大鼠心室肌制备培养搏动心肌细胞， １８ ｈ后接种 １００ ＴＣＩＤ５０的 ＣＶＢ３作为实验性病毒性心肌炎模型，并采用放射性同位素４５Ｃａ２＋示踪技术，观察了 １～２０ ｍｍｏｌ／ Ｌ牛磺酸对正常及感染 ＣＶＢ３后心肌细胞 Ｃａ２＋内流的影响。结果：（ｌ）１０～２０ ｍｍｏｌ／ Ｌ牛磺酸对正常心肌细胞不同胞外 Ｃａ２＋浓度（［Ｃａ２＋］０， ０．５、 １．５和 ４．０ ｍｍｏｌ／ Ｌ）下的 Ｃａ２＋内流均有抑制作用，而 １ｍｍｏｌ／ Ｌ牛磺酸只抑制高［Ｃａ２＋］０（４．０ ｍｍｏｌ／ Ｌ）时 Ｃａ２＋内流，对低［Ｃａ２＋］０（０．５ ｍｍｏｌ／ Ｌ）和正常［Ｃａ２＋］０（１．５ ｍｍｏｌ／ Ｌ）时 Ｃａ２＋内流无明显作用；（２） ｌ～２０ ｍｍｏｌ／ Ｌβ－丙氨酸对 Ｃａ２＋内流无明显影响；（３）感染ＣＶＢ３后Ｃａ２＋内流增加，加用１ｍｍｏｌ／ Ｌ牛磺酸后能减少感染ＣＶＢ３后的Ｃａ２＋内流。结论：牛磺酸具有抑制培养心肌细胞感染ＣＶＢ３后Ｃａ２＋内流的作用，这可能是牛磺酸能减轻ＣＶＢ３所致细胞损伤的机理之一。     

大鼠主动脉α_1肾上腺素能受体激活引起Ca~（2＋）内流的特性

大鼠主动脉α_１肾上腺素能受体激活引起Ｃａ~（２＋）内流的特性南通医学院药理学教研室徐济良等在大鼠主动脉平滑肌标本上，钙通道阻断剂──硝苯吡啶（０．５μｍｏｌ·Ｌ－１）能完全阻断由ＫＣｌ（１００ｍｍｏｌ·Ｌ－１）引起的血管收缩和４５Ｃａ内流，并部分抑制...     

海风藤醇B对PAF诱导的兔血小板钙内流和胞内游离钙浓度升…

应用＾４５Ｃａ＾２＋和钙荧光指示剂Ｑｕｉｎ－２／ＡＭ进行实验，发现海风藤醇Ｂ（１０，１００μｍｏｌ．Ｌ＾－１）无论对血小板激活因子（ＰＡＦ）引起的兔洗涤血小板Ｃａ＾２＋内流还是胞内游离钙浓度（Ｃａ＾２＋）升高均有抑制作用，且呈良好的剂量相关，最大抑制率分别为３７．２％和５０．８％，但对Ａ２３１８７引起的胞内（Ｃａ＾２＋）升高无显著抑制作用。结果表明，海风藤醇Ｂ能选择性拮抗ＰＡＦ诱导的钙内流的Ｃａ＾     

海风藤醇B对PAF诱导的兔血小板钙内流和胞内游离钙浓度升高的抑制作用

应用４５Ｃａ２＋和钙荧光指示剂Ｑｕｉｎ－２／ＡＭ进行实验，发现海风藤醇Ｂ（１０、１００μｍｏｌ·Ｌ－１）无论对血小板激活因子（ＰＡＦ）引起的兔洗涤血小板Ｃａ２＋内流还是胞内游离钙浓度（［Ｃａ２＋］ｉ）升高均有抑制作用，且呈良好的剂量相关，最大抑制率分别为３７．２％和５０．８％；但对Ａ２３１８７引起的胞内［Ｃａ２＋］ｉ升高无显著抑制作用。结果表明：海风藤醇Ｂ能选择性拮抗ＰＡＦ诱导的钙内流和［Ｃａ２＋］ｉ的升高。     

钙离子与牛磺酸两者跨心肌细胞膜内流的相互影响(摘要)

目的观察钙离子与牛磺酸跨心肌细胞膜内流的相互影响。方法取新生ＳＤ大鼠心室肌制备培养搏动心肌细胞,采用放射性同位素４５Ｃａ２＋及３Ｈ－牛磺酸示踪技术。结果①牛磺酸内流在低胞外Ｃａ２＋浓度（［Ｃａ２＋］）００．５ｍｍｏｌＬ）和高［Ｃａ２＋］０（４．０ｍｍｏｌＬ）均比正常［Ｃａ２＋］０（１．５ｍｍｏｌＬ）和高［Ｃａ２＋］０（４．０ｍｍｏｌＬ）时增加,尤以低［Ｃａ２＋］０时明显;异搏定（１０μｍｏｌＬ）能促进牛磺酸的内流;②１０～２０ｍｍｏｌＬ牛磺酸对不同［Ｃａ２＋］０（０．５、１．５和４．０ｍｍｏｌＬ）下的Ｃａ２＋内流均有抑制作用,而１ｍｍｏｌＬ牛磺酸只抑制高［Ｃａ２＋］０时Ｃａ２＋内流,对低［Ｃａ２＋］０和正常［Ｃａ２＋］０时Ｃａ２＋内流无明显作用;１～２０ｍｍｏｌＬβ－丙氨酸对Ｃａ２＋内流无明显影响。结论胞外Ｃａ２＋浓度的变化可直接影响牛磺酸内流,而牛磺酸能抑制Ｃａ２＋的内流,两者相互影响,从而发挥牛磺酸调节细胞内Ｃａ２＋浓度的作用。     

黄腐酸和超氧阴离子对软骨细胞内钙离子浓度的影响

目的：为探讨病区黄腐酸（ＦＡ）和活性氧自由基可能引起大骨节病，我们测定了在ＦＡ和超氧自由基（）作用下，软骨细胞内钙离子浓度（［Ｃａ￣（２＋）］ｉ）随时间的变化。方法：应用萤光指示剂Ｆｕｒａ－２／ＡＭ测定细胞内钙离子浓度并用下式计算：［Ｃａ￣（２＋）］ｉ＝Ｋｄ（Ｆ－Ｆ＿（ｍｉｎ））／（Ｆ＿（ｍａｘ）－Ｆ）。结果：作用４５ｍｉｎ后，［Ｃａ￣（２＋）］ｉ从１．６２×１Ｏ￣（－７）ｍｏｌ／Ｌ升达１．１８×１０￣（－６）ｍｏｌ／Ｌ；ＦＡ作用４ｈ后，［Ｃａ￣（２＋）］ｉ从３．７８×１０￣（－７）ｍｏｌ／Ｌ升达５．５１×１０￣（－７）ｍｏｌ／Ｌ。结论：说明ＦＡ与·有相似的促进［Ｃａ￣（２＋）］ｉ升高的作用，［Ｃａ￣（２＋）］ｉ的升高将造成软骨细胞损伤，而软骨坏死是大骨节病的重要病理特症之一。     

血管紧张系Ⅱ受体基因敲除对跨膜钙内流的作用

目的 观察血管紧张素Ⅱ受体亚型（ＡＴ１ａ）基因敲除对跨膜钙内流的影响。方法 培养ＡＴ１ａ基因敲除及其野生型对照小鼠的主动脉血管平滑肌细胞（ＶＳＭＣ）和应用荧光倒置显微镜及钙荧光指示剂Ｆｕｒａ－２／ＡＭ动态观测ＶＳＭＣ钙离子（Ｃａ＾２＋）ｉ变化。结果 在血管紧张素Ⅱ（ＡｎｇⅡ）刺激下钙内流显著增加,ＡＴ１ａ敲除组ＶＳＭＣ钙净增值为（２０４±２２）ｎｍｏｌ／Ｌ,基础（Ｃａ＾２＋）ｉ为（１０８±９）ｎｍ     

外源性神经节苷脂GM_3对Ca~（2＋）－ATP酶及红细胞胞浆Ca~（2＋）－浓度的影响

研究神经节苷脂ＧＭ３（简称ＧＭ３）对部分纯化的人红细胞膜Ｃａ２＋－ＡＴＰ酶的作用和对完整兔红细胞浆［Ｃａ２＋］的影响。结果表明：外源性ＧＭ３对Ｃａ２＋－ＡＴＰ酶的作用呈浓度依赖性双相调节即浓度为１～６．５μｍｏｌ／Ｌ时抑制酶活性，浓度大于６．５μｍｏｌ／Ｌ时激活酶活性；ＧＭ３不影响钙调素（ＣａＭ）对酶的激活；ＣＭ３对兔红细胞浆［Ｃａ２＋］也呈浓度依赖性双相调节即在ＧＭ３浓度低于６９μｍｏｌ／Ｌ时［Ｃａ２＋］有不同程度升高，浓度大于６０μｍｏｌ／Ｌ时则降低［Ｃａ２＋］。     

应用Fura-2/AM测定兔视网膜细胞内游离钙的方法

目的：建立适宜条件下，用荧光指示剂Ｆｕｒａ－２测定乳兔视网膜细胞内游离钙（简称［Ｃａ２＋］ｉ）的方法。方法：用酶解制备视网膜细胞悬液。Ｆｕｒａ－２／ＡＭ负载进行荧光测定。结果：经０．０５％胰蛋白酶消化１０分钟，可使细胞存活率达９０％以上。在３７℃条件下与Ｆｕｒａ－２／ＡＭ温育４０分钟，于３０分钟内测定为最佳条件。结论：静息状态下（［Ｃａ２＋］ｉ）水平为（２２３±２７）ｎｍｏｌ／Ｌ，其值在文献报道范围内。高钾去极化，在Ｋ＋为２５ｍｍｏｌ／Ｌ和５０ｍｍｏｌ／Ｌ时，分别使（［Ｃａ２＋］ｉ）增加了５９％和１４８％，由此证明视网膜细胞悬液制备和测定方法是可行的。     

甲基黄酮醇胺抗血栓形成的机理研究

采用生物鉴定法测定甲基黄酮醇胺（ＭＦＡ）对ＰＧＩ２和ＴＸＡ２样物质生成的影响。以血小板聚集率％表示大鼠颈总动脉环ＰＧＩ２活性，ＭＦＡ（２４．８μｍｏｌ／ｋｇ，ｉｖ）组，阿斯匹林（ＡＳＡ，０．８３ｍｍｏｌ／ｋｇ，ｉｖ）组和溶媒对照组分别为０．４７±０．１９、０．１８±０．１６、０．５０±０．１３／ｍｇ，结果提示：ＭＦＡ不抑制ＴＸＡ２的生成（Ｐ＜０．０５）；ＡＳＡ明显抑制ＰＧＩ２的生成（Ｐ＜０．０１）。采用表面灌流法，ＡＡ为诱导剂，以兔主动脉条收缩强度（ｇ）表示ＴＸＡ２样物质的活性，ＭＦＡ（１０ｍｍｏｌ／Ｌ）组，咪唑（１．６７ｍｍｏｌ／Ｌ）组和溶媒对照组分别为０．３８±０．１３、０．１７±０．０９和０．６９±０．２２ｇ，结果提示ＭＦＡ和咪唑抑制ＴＸＡ２样物质的生成（Ｐ＜０．０１）。采用放射免疫法测定，ＭＦＡ６．２μｍｏｌ或１２．４μｍｏｌ／ｋｇ能明显抑制心肌梗塞家兔ＴＸＢ２的升高（Ｐ＜０．０１），而对６－ｋｅｔｏ－ＰＧＦ１α无明显影响     

三七皂甙单体Rb1对动脉平滑肌钙离子内流的影响

本文用核素~(45)Ca示踪法观察了三七皂甙单体Rb1对兔主动脉平滑肌钙离子内流的影响。结果显示:Rb1(10~(-5)mol/L)对正常营养液的主动脉平滑肌钙离子跨膜流动无明显影响,但对高钾(140mmol/L)或去甲肾上腺素(10~(-5)mol/L)引起的主动脉平滑肌钙离子内流却有明显的抑制作用(P<0.01)。提示三七皂甙Rb1对血管平滑肌有钙拮抗性作用。     

Nerve Growth Factor Inhibits Gd^3＋ -sensitive Calcium Influx and Reduces Chemical Anoxic Neuronal Death

To investigate whether glutamate and voltage-gated calcium channels-independent calcium influx exists during acute anoxic neuronal damage and its possible relationship to neuronal protective function of NGF. In in vitro model of acute anoxia, hippocampal cultures from newborn rats were exposed to 3 mmol/L KCN. Changes of intracellular Ca^2＋ concentration （[Ca^2＋]i） were monitored by con-focal imaging and cell viability was assayed by PI and cFDA staining. The results showed that after treatment with primary hippocampal cultures with 3 mmol/L KCN for 15 min, [Ca^2＋]i was significantly increased 6.27-fold compared to pre-anoxia level and 73.3% of the cells died. When combination of 20 μmol/L MK-801 （glutamate receptor antagonist）, 40 μmol/L CNQX （AMPA receptor antagonist） and 5 μmol/L nimodipine （voltage-gated calcium channel antagonist） （hereafter denoted as MCN） were administrated to hippocampal cultures, levels of [Ca^2＋]i and cell death rate induced by KCN were partially reduced by 35.9% and 47.5% respectively. However, Gd^3＋ （10 μmol/L） almost completely blocked KCN-mediated [Ca^2＋]i elevation by 81.9% and reduced neuronal death by 88.8% in the presence of MCN. It is noteworthy that NGF, used in combination with MCN, inhibited KCN-induced [Ca^2＋]i increase by 77.4% and reduced cell death by 87.1%. Only PLC in- hibitor U73122 （10 μmol/L） abolished NGF effects. It is concluded that Gd^3＋-sensitive calcium influx, which is NMDA （glutamate receptor） and voltage-gated calcium channels-independent, is responsible for acute anoxic neuronal death. NGF can inhibit Gd^3＋-sensitive calcium influx and reduce anoxic neuronal death through activating PLC pathway.     

Both Hypoxic Endothelial Cell Conditioned Medium and Hypoxia Elevate Intracellular Free Calcium in Pulmonary Artery Smooth Mu

ＢｏｔｈＨｙｐｏｘｉｃＥｎｄｏｔｈｅｌｉａｌＣｅｌｌＣｏｎｄｉｔｉｏｎｅｄＭｅｄｉｕｍａｎｄＨｙｐｏｘｉａＥｌｅｖａｔｅＩｎｔｒａｃｅｌｌｕｌａｒＦｒｅｅＣａｌｃｉｕｍｉｎＰｕｌｍｏｎａｒｙＡｒｔｅｒｙＳｍｏｏｔｈＭｕｓｃｌｅＣｅｌｌｓＨＵＱｉｎｇ－...     

罗哌卡因对大鼠离体主动脉收缩作用的钙离子调节机制

目的〓〖HTK〗研究Ca2+在罗哌卡因（ropivacaine）所致血管收缩反应中的调节作用。〖HTW〗方法〓〖HTK〗用等张肌力测定仪和Ca2+ 荧光分光光度计分别测定Wistar大鼠去内膜主动脉血管环和血管段对累积剂量罗哌卡因的收缩反应和细胞内Ca2+浓度（［Ca2+］i）的变化；并观察Ca2+通道阻滞剂尼卡地平(nicardipine)、肌质网三磷酸肌醇受体阻滞剂2-APB和细胞外液低浓度Ca2+对累积剂量罗哌卡因诱发的收缩反应和［Ca2+］i的影响。〖HTW〗结果〓〖HTK〗罗哌卡因诱发剂量关联性双相收缩反应：低浓度（0.03～0.3mmol/L）时肌张力逐渐增强，高浓度（1～3 mmol/L）时收缩张力依次回落。罗哌卡因所产生的这一收缩效应可分别被尼卡地平(1, 5, 10nmol/L)、2-APB (5, 10, 50μmol/L)和营养液中低浓度Ca2+（2, 1和0mmol/L）相关性抑制。罗哌卡因诱发与肌张力变化规律相同的双相［Ca2+］i升高；尼卡地平(10nmol/L)和2-APB(50μmol/L)预处理及营养液中去除Ca2+，明显降低罗哌卡因所诱发的［Ca2+］i的升高幅度。〖HTW〗结论〓〖HTK〗细胞外Ca2+内流和肌质网Ca2+释放所致的［Ca2+］i升高参与了罗哌卡因诱发的血管平滑肌收缩反应。     

Kv1.1及Kv1.3通道亚型对小鼠肠系膜微细动脉的调节作用

目的 研究Kv1.1及Kv1.3通道亚型对小鼠肠系膜微细血管的调节作用.方法 以健康6～8周C57BL/6雄性小鼠肠系膜微细动脉作为研究对象,应用丹麦DMT520A离体微血管张力测定系统记录血管张力变化.应用广谱电压依赖性钾通道(Kv)阻断剂4-AP,Kv1.3通道选择性阻断剂PAP-1,Kv1.1通道选择性阻断剂TEA分别作用于静息状态,KCl及NE预收缩动脉,记录血管张力变化情况.应用Kv通道阻断剂4-AP,Kv1.3通道选择性阻断剂PAP-1作用于血管,观察Kv及Kv1.3通道在0 mmol/L Ca2+及2 mmol/L Ca2+ K-H液中对NE收缩曲线的作用.结果 Kv通道阻断剂4-AP可引起静息状态的血管收缩,并进一步收缩KCl预收缩的血管,但浓度依赖性舒张NE预收缩的动脉,并且与对照组相比,4-AP能明显抑制NE在0 mmol/L Ca2+液中所致的血管收缩[(3.45-±0.24)mN vs(0.11±0.02) mN,P＜0.01].Kv1.3通道选择性阻断剂PAP-1未能收缩静息状态的血管,但可使KCl预收缩的血管发生轻微舒张反应,却明显舒张NE预收缩的动脉,而且PAP-1既可抑制NE在0 mmol/L Ca2+ K-H液中所致的血管收缩[对照组vs PAP-1组:(4.28 ±0.53)mN vs(2.75 ±0.49)mN,P＜0.05],又可抑制在2 mmol/L Ca2+液中的收缩张力[对照组vsPAP-1组:(7.08 ±0.58)mN vs(5.90 ±0.80)mN,P＜0.05].Kv1.1通道选择性阻断剂TEA可引起静息状态的血管收缩,但在0 mmol/L Ca2+液中该作用消失,同时对KCl或NE预收缩的动脉均无明显作用.结论 Kv通道可调节小鼠肠系膜动脉的舒缩反应.其中Kv1.1通道主要发挥血管收缩调节作用,可能与促进血管平滑肌细胞外钙内流有关,而Kv1.3通道主要发挥血管舒张调节作用,可能同时抑制平滑肌细胞内钙释放和细胞外钙内流.     

乙醇对颈上神经元细胞内外钙信号的双重作用

目的:探讨乙醇对原代培养颈上神经节神经元(SCGs)细胞质钙稳态的影响。方法:分散、培养新生12 h内大鼠SCGs,应用激光共聚焦显微技术,观察不同浓度乙醇对SCGs细胞质Ca2+浓度([Ca2+]i)的作用。结果:KCl及钙离子载体A23187所诱发的[Ca2+]i增高,可被乙醇(100 mmol/L)显著抑制,但是乙醇(30,100,600 mmol/L)自身却可浓度依赖性增加[Ca2+]i,并且使用无Ca2+外液和氯化镉对该增加作用无影响。结论:乙醇可抑制细胞外Ca2+内流,同时增加细胞质[Ca2+]i,来源可能是胞内钙库的释放。     

氯胺酮对大鼠心肌细胞钙离子移动的影响

目的研究不同浓度氯胺酮对KCl诱发的大鼠心肌细胞钙离子移动的影响，探讨其对心肌收缩力的作用。方法用Fluo-3AM钙荧光指示剂染色急性分离的大鼠心肌细胞，在激光共聚焦显微镜下动态测定用药前和使用浓度为1×10     

安定对兔离体气管平滑肌收缩力的影响

为了对有气道高反应的患者选用理想的镇静安定药提供参考依据,采用研究不同浓度的安定对氯化钾、乙酰胆碱、电脉冲3种刺激因素诱发兔离体气管子滑肌收缩影响的方法。结果：0．018mmol／L的安定无明显抑制作用（P＞0．05）,0．18mmol／L和0．36mmol／L的安定可显著抑制这3种刺激因素诱发的气管平滑肌收缩（P＜0．05或P＜0．01）,β受体阻滞剂普萘乐尔和中枢性苯二氮受体阻滞剂氟马西尼不能拮抗安定对气管平滑肌收缩的抑制作用。结论：安定对兔离体气管平滑肌张力有显著的抑制作用,其部分作用机制与抑制外钙内流和内钙释放及抑制蛋白激酶C（PKC）信号传导系统有关。     

Effect of crystalloid cardioplegic solution at different calcium concentration on immature myocardium

OBJECTIVE To determine the myocardial protective effect of crystalloid cardioplegic solution at different calcium concentration on immature myocardium.

METHODS Isolated perfused neonatal rabbit hearts from three groups, arrested by intermittent infusion of St. Thomas II cardioplegic solution with different concentration of calcium (in each group, only calcium concentration of cardioplegic solution was modified, I. [Ca2+] 0.6 mmol/L; II. [Ca2+] 1.2 mmol/L; III. [Ca2+] 2.4 mmol/L), were kept ischemic globally at 20 degrees C for 90 minutes and then followed by 30 minutes of reperfusion in Langendorff mode.

RESULTS Although the recovery of LVDP, +dp/dtmax at calcium content of 2.4 mmol/L after 10 minutes of reperfusion was significantly higher than those at 0.6 and 1.2 mmol/L calcium (P < 0.05, P < 0.01, respectively). The declined tendency of left ventricular hemodynamics after 20 minutes of reperfusion in this group was detected. By the end of reperfusion, the left ventricular functional recovery at 2.4 mmol/L calcium did not differ from those at 1.2 and 0.6 mmol/L calcium. Conversely, postischemic left ventricular functions at 0.6 and 1.2 mmol/L calcium were gradually improved during 30 minutes of reperfusion. In 2.4 mmol/L calcium group, the Ca(2+)-ATPase activity significantly increased (P < 0.01, P < 0.001) whereas myocardial ATP content was lower when compared with 1.2 mmol/L (P < 0.001) and 0.6 mmol/L calcium groups.

CONCLUSIONS Our research demonstrated that there were no statistical differences with respect to hemodynamic recovery in three groups after 30 minutes of reperfusion although left ventricular functional recovery at 2.4 mmol/L calcium accelerated early after reperfusion. In addition, with 2.4 mmol/L calcium, myocardial ATP content was decreased significantly. We conclude that, from the point of view of myocardial energy metabolism, St. Thomas II cardioplegic solution at high concentration of calcium can not provide immature myocardium with optimal myocardial protection while with 1.2 mmol/L calcium, however, better high-energy store can be preserved.

     

晶体停搏液中钙离子浓度对幼兔未成熟心肌的保护作用

OBJECTIVE: To determine the myocardial protective effect of St. Thomas II cardioplegia at different calcium concentration on immature myocardium. METHODS: Isolated perfused neonatal rabbit hearts from three groups (the calcium concentration of St. Thomas II cardioplegia was modified: [Ca2+] 0.6 mmol/L; [Ca2+]1.2 mmol/L; [Ca2+]2.4 mmol/L) were subjected to 20 degrees C hypothermia, 90 minutes of global ischemia followed by 30 minutes reperfusion in Langendorff mode. RESULTS: Although the recovery of LVDP, +/- dp/dtmax at calcium content of 2.4 mmol/L after 10 minutes of reperfusion was significantly higher than that at 0.6 and 1.2 mmol/L calcium (P < 0.05, P < 0.01, respectively), the declined tendency of left ventricular hemodynamics in this group was detected after 20 minutes of reperfusion. By the end of 30-minute reperfusion, the left ventricular hemodynamic recovery at 2.4 mmol/L calcium did not differ from those at 0.6 mmol/L and 1.2 mmol/L calcium. Conversely, postischemic left ventricular functions at 0.6 and 1.2 mmol/L calcium were gradually improved during the 30 minutes reperfusion. Ca(2+)-ATPase activity at 2.4 mmol/L calcium showed significant increase (P < 0.01, P < 0.001), whereas ATP content was lower than that of other groups. CONCLUSION: Calcium accumulated in extracellular space during ischemia enters myocardial cell via Ca2+ channel and Ca2+/Na+ exchange after reperfusion, activates Ca(2+)-ATPase, and finally accelerates adenosinetriphosphate (ATP) consumption induced by calcium, which would be responsible for the results of our study. We conclude that, from the point of view of myocardial cell energy metabolism, St. Thomas II cardioplegia at high calcium concentration can not provide immature myocardium with optimal myocardial protection.