超极化停搏对体外循环中心肌细胞膜微粘度变化的影响

目的比较超极化停搏和去极化停搏对体外循环(CPB)中心肌细胞膜流动性变化的影响,评价超极化停搏液的心肌保护作用. 方法根据随机数字表法将72只家猫均分为3组,每组24只.对照组:不阻断上、下腔静脉和主动脉,仅行并行循环180分钟;去极化停搏组:阻断主动脉60分钟,再灌注90分钟,心脏停搏液使用St.Thomas液(K 16mmol/L);超极化停搏组:心脏停搏液使用含吡那地尔的St.Thomas液(K 5mmol/L),其余处理与去极化停搏组相同.应用荧光偏振法测定心肌细胞膜的微粘度(η),以η的倒数表示心肌细胞膜流动性. 结果去极化停搏组主动脉阻断期间心肌细胞膜η值明显上升,且于再灌注期间进一步升高;超极化停搏组主动脉阻断期间亦呈升高趋势,但各时间点η值均明显低于去极化停搏组(P＜0.01). 结论超极化停搏比去极化停搏能更有效地维持CPB中缺血-再灌注心肌细胞膜的流动性,从而起到更好的心肌保护作用.     

血液超极化停搏对体外循环缺血心肌保护的研究

目的：评价含ATP敏感性钾通道开放剂吡那地尔的血液停搏液诱导的心脏起极化停搏在常温与低温体外循环下对缺血心肌的保护效果。方法：18只犬随机分为对照组（A组）、常温血液超极化组（B组）、低温血液超极化组（C组）,每组6只。对照组以4℃标准St.Thomas液（K^ 16mmol/L)为心脏停搏液,常温血液超极化组和低温血液超极化组分别以含吡那地尔50μmol/L的37℃St.Thomas液（K^ 5mmol/L,含血比例1：1）和含吡那地尔50μmol/L和4℃St.Thomas液（K^ 5mmol/L,含血比例1：1）为心脏停搏液。体外循环期间,A组和C组温度保持在26℃-28℃,B组温度保持在35℃-37℃。三组体外循环（CPB）期间,均全心缺血60min,恢复灌注30min。对比观察阻断升主动脉前、后心肌腺苷酸（ATP、ADP、AMP、TAN、EC）含量、心肌超微结构、脂质过氧化物丙二醛（MDA）含量以及血液动力学多项参数的变化。结果：对照组在阻断50min和开放30min,心肌各项指标均显示有明显的缺血和再灌注损害;而血液超极化组损害较轻,特别是低温血液超极化组,损害最轻。结论：含吡那地尔的血液停搏液诱导的超极化停搏,其心肌保护效果明显优于传统的高钾去极化停搏;低温血液超极化停搏又优于常温血液超极化停搏。     

吡那地尔预处理对体外循环犬心肌的保护效果

目的 探讨ATP敏感性钾通道开放剂(KCOs)吡那地尔(Pinacidil)药物预处理对常温及低温犬体外循环(CPB)晶体高钾停搏液间断灌注心肌的保护效果。方法 18条犬随机分为三组,每组6条,分别建立犬的常温及低温CPB全心缺血Pinacidil预处理模型。对照组(A组):低温CPB,主动脉根部灌注4℃St.Thomas停搏液(K~+16mmol/L)10ml/kg,阻断30min复灌一次(1/2首量);B组:常温CPB,主动脉根部灌注37℃含氧Pinacidil液(0.083mg/kg);C组:低温CPB,主动脉根部灌注液同B组。三组心脏均接受60min缺血和30min再灌注。阻断主动脉前,开放后15min、30min测血液动力学改变;并循环5min,阻断循环30min、60min及开放循环20min于左心室取心肌组织,测定心肌腺苷酸含量。结果 再灌注期间C组的血液动力学指标明显好于A、B组(P<0.01),而B组又较A组好(P<0.01)。缺血及再灌注期间C组心肌的ATP含量也明显高于A、B组(P<0.01),B组又高于A组(P<0.01)。结论 Pinacidil预处理时对CPB下缺血心肌具有良好的保护效果,低温的效果优于常温。     

吡那地尔超极化心脏停搏液对再灌注后细胞因子及心脏功能的影响

目的观察犬体外循环(CPB)再灌注后吡那地尔超极化心脏停搏液与传统高钾心脏停搏液对肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和心脏功能的影响. 方法 12只雄性杂种狼犬随机分为两组,对照组(n=6)主动脉阻断时用4℃ St.Thomas Ⅱ号心脏停搏液(K+ 20 mmol/L),每30分钟灌注1次;实验组(n=6)用4℃含吡那地尔50 μmol/L 的St.Thomas Ⅱ号心脏停搏液(K+ 5 mmol/L),每50分钟灌注1次.两组犬主动脉均阻断150分钟.在转流前和主动脉开放后180分钟时测定TNF-α和IL-6的含量,于转流前、主动脉开放后30、60、120和180分钟时监测血流动力学指标的变化. 结果主动脉开放后180分钟,两组TNF-α和IL-6与转流前比较均明显升高(P<0.01),但两组间比较差别无显著性意义.主动脉开放后120分钟和180分钟,两组平均动脉压(MAP)、心脏指数(CI)、每搏指数(SI)、左心室每搏作功指数(LVSWI)与转流前比较均明显降低(P<0.05),但两组间差别无显著性意义. 结论与传统高钾心脏停搏液比较,吡那地尔超极化心脏停搏液无明显的减轻炎性反应作用,其改善心功能的作用也并不优于传统的高钾心脏停搏液.     

心肺转流中吡那地尔超极化停搏液对实验犬冠脉流量的影响

目的　观察心肺转流 (CPB)中吡那地尔超极化停搏液与传统高钾停搏液对犬冠脉流量的影响。方法　 12条雄性杂种狼犬 ,随机分为两组 ,对照组 (Ⅰ组 ) :心肌保护液灌注 4℃St.Thomas停搏液 (K+ 2 0mmol/L) ,每 30分钟一次 ;实验组 (Ⅱ组 ) :心肌保护液灌注 4℃含吡那地尔 5 0 μmol/L的St.Thomas停搏液 (K+ 5mmol/L) ,每 5 0分钟一次。两组犬主动脉均阻断 15 0min并分别于CPB前、再灌注后 10、30、6 0min时测定冠脉流量 ,同时监测围术期血液动力学。结果　与CPB前比较 ,Ⅱ组在再灌注后 10min冠脉血流量明显增加 ,再灌注后 30min进一步增加 ,且在再灌注后 6 0min继续维持在高流量水平 ,而Ⅰ组只有在再灌注 6 0min时 ,冠脉流量有所增加 (P <0 0 5 ) ;在再灌注后的各个时点 ,Ⅱ组的冠脉流量远远高于Ⅰ组 (P <0 0 5 ) ,两组之间血液动力学指标无显著性差异 (P >0 0 5 )。结论　吡那地尔可明显增加实验犬的冠脉流量 ,而冠脉流量的增加可能与其心功能的恢复无关     

吡那地尔超极化停搏对大鼠离体心脏缺血再灌时心肌线粒体损伤的影响

目的探讨吡那地尔超极化停搏对大鼠离体心脏缺血再灌注时心肌线粒体损伤的影响。方法健康雄性SD大鼠,成功建立Langendorff再灌注模型的80个心脏随机分为5组：对照组（C组）、去极化停搏组（D组）、吡那地尔超极化停搏组（H组）、线粒体ATP敏感性钾通道阻滞剂5-羟葵酸（5-HD）＋去极化停搏组（5-HD＋D组）和5-HD＋吡那地尔超极化停搏组（5-HD＋H组）。以K-H液平衡灌注20 min后（平衡末）,C组阻断主动脉,不予停搏液灌注,使其自然停搏,D组用37℃ST.ThomasⅡ停搏液灌注,H组用37℃超极化停搏液灌注,5-HD＋D组和5-HD＋H组分别用含有100μmol/L 5-HD的37℃ST.ThomasⅡ停搏液或超极化停搏液20 ml/kg灌注,缺血40 min。分别于平衡末及再灌注30 min时取8个心脏,测定心肌线粒体呼吸功能指标[4态呼吸耗氧速率、3态呼吸耗氧速率、呼吸控制率（PCR）及磷氧比（P/O）]、线粒体酶（NADH氧化酶、琥珀酸氧化酶和细胞色素C氧化酶）活性及线粒体膜电位（MMP）,电镜下观察线粒体的超微结构。结果与平衡末比较,各组再灌注30 min时心肌线粒体呼吸功能指标（3态呼吸耗氧速率、PCR及P/O）、线粒体酶活性及MMP降低（P〈0.05或0.01）;与C组比较,再灌注30 min时其余各组上述指标均升高（P〈0.01）;再灌注30 min时H组线粒体的功能及病理损伤最轻。结论吡那地尔超极化停搏能明显改善大鼠离体心脏缺血再灌注时心肌线粒体功能,减轻线粒体超微结构损伤,其机制与开放线粒体ATP敏感性钾通道有关。     

心肺转流下犬心肌c-fos基因的表达

目的　研究冷心脏停搏液心肺转流 (CPB)下犬心肌损伤与c fos基因的表达。方法　10只犬分为实验组 (I组 ,n =6 )和对照组 (II组 ,n =4 )。I组动物施行全身低温心脏深低温 4℃St.Thomas液顺行灌注心停搏CPB ,II组动物在常温下施行不停跳并行循环。取不同时点的右心房组织进行免疫组化分析及透射电镜观察。结果　并行循环前 ,两组动物心肌细胞均无Fos阳性核染色 ;血管内皮细胞均有少量阳性染色。I组主动脉阻断 6 0min、主动脉开放 2 0及 4 0min心肌细胞核Fos阳性率持续增加 ;各时点血管内皮细胞Fos阳性率明显增加 ,且以主动脉开放 4 0min最高。II组并行循环 10 0min时 ,心肌细胞及血管内皮细胞Fos阳性率与并行前比较差异显著 (P <0 0 1) ,而显著低于I组同时点。I组开放主动脉 4 0min时心肌超微结构存在损伤征象。结论　 (1)冷心脏停搏液CPB下心肌存在一定的缺血 再灌注损伤 ;缺血和 (或 )低温诱导c fos的表达 ,再灌注则显著诱导心肌c fos的表达 ;(2 )血管内皮细胞c fos表达较心肌细胞迅速和强烈 ;(3)CPB本身亦可能诱导c fos基因的表达 ;(4)c fos表达增加与心肌损伤有关     

极化型心脏停搏液研究进展

现代心脏手术中常规应用高钾溶液使心脏停搏.高钾停搏液的代表是St.Thomas液.其中的高钾成分使心肌细胞膜去极化,跨膜电位降低,不能形成和传播动作电位,心脏处于舒张期停搏.但细胞膜的去极化会导致持续性Na+/Ca2+窗口电流离子交换,引起持续性能量消耗和Ca2+超载,致使线粒体损伤、细胞死亡,引发术后心功能不良和缺血再灌注损伤[1].理想的心脏停搏液应使心肌细胞的跨膜电位处于极化状态,从而关闭离子通道,达到避免离子失衡和继发损伤的目的.细胞膜去极化程度越小,心肌保护的效果就越好,再灌注损伤的的程度就越轻[2].     

心脏超极化与去极化联合停搏液对心肌的保护作用

虽然含有钾通道开放剂(KCOs)的超极化停搏液对缺血心肌的保护效果优于传统的去极化停搏液[1],但是去极化停搏液停跳速度快,已在临床应用多年.本文旨在观察超极化停搏液联合去极化停搏液对缺血心肌的保护效果.     

心脏超极化与去极化联合停博液对心肌的保护作用

虽然含有钾通道开放剂(KCOs)的超极化停搏液对缺血心肌的保护效果优于传统的去极化停搏液[1],但是去极化停搏液停跳速度快,已在临床应用多年。本文旨在观察超极化停搏液联合去极化停搏液对缺血心肌的保护效果。     

钾通道开放剂心脏超极化停搏保护效果的研究

目的 对比观察大量三磷酸腺苷（ＡＴＰ）敏感性钾通道开放剂吡那地尔对常温／低温体外循环（ＣＰＢ）心脏超极化停跳缺血心肌的保护作用。方法 １８只犬随机分３组,每组６只,低温超极化组（ＬＨ）：阻断升主动脉后,心脏灌注４℃含吡那地尔停跳液,ＣＰＢ血温为２６～２８℃,开放前复温至３７℃,全心缺血６０ｍｉｎ,恢复灌注３０ｍｉｎ;常温超极化组（ＷＨ）：ＣＰＢ血温３５～３７℃,心脏灌注３７地７０含吡那地尔（５０μｍｏｌ／Ｌ）停跳液,余同ＬＨ组;对照组（Ｃ）;无吡那地尔的标准Ｓｔ、Ｔｈｏｍａｓ停跳液,余３７℃含昆那地尔（５０ｕｍｏｌ／Ｌ）停跳液,余同ＬＨ组;对照组（Ｃ）：无吡那地尔的标准Ｓｔ．Ｔｈｏｍａｓ停跳液,余同ＬＨ组,对比观察吡那地尔心脏超极化停跳不同时相各项指标的变化。结果 （１）停复跳情况：ＬＨ组、Ｃ组灌注后心脏停跳较     

药物预处理与诱导超极化对离体心脏的保护研究

目的：探讨AT敏感性钾通道开放剂（KCOs)吡那地尔对Langendorff灌注兔心脏模型药物预处理与药物诱导超极化停跳的保护作用。方法：离体兔心40个,随机等分5组。对比研究2种浓度吡那地尔在4℃或37℃全心缺血40min,复灌20min的心肌组织腺苷酸含量,脂质过氧化物的变化,以及再灌注后10、20min心功能恢复的情况。结果（1）心脏诱导停跳以4℃超极化与药物预处理组迅速,37℃超极化组较为缓慢;再灌注后仅对照组心脏复跳较慢。（2）与对照组同期比较,比吡那地尔预处理以及超极化的心脏再灌注后心肌收缩力与左心室内压恢复较快,其中心肌收缩力的恢复更为显著;（3）再灌注后,对照组心肌ATP、总腺苷量、细胞能荷水平低于预处理与超极化组（P＜0．05或0．01）其中以37℃预处理ATP含量较高,而经吡那地尔处理的4组,丙二醛则不同程度的低于对照组,结论：吡那地尔诱导心脏超极化停跳以及药物预处理,有助于降低心肌ATP的消耗,减少脂质过氧化物的形成,明显改善离体兔心脏缺血／再灌注后期心功能。     

缺血预适应对缺血-再灌注心肌细胞的保护作用

目的观察缺血预处理（IPC）对心肺转流（CPB）中缺血-再灌注心肌损伤及心功能恢复的影响。方法将72只健康家猫随机均分为：单纯CPB组、缺血-再灌注组和IPC组。在猫CPB模型的基础上,测定猫心肌丙二醛（MDA）含量、血清乳酸脱氢酶（LDH）水平和心肌组织磷脂酶A2（PLA2）活性的变化,观察术中心功能的变化。结果IPC组CPB中的血清LDH浓度、心肌MDA含量和心肌组织PLA2活性均明显低于缺血-再灌注组,心脏复跳后各心功能指标的恢复明显优于缺血-再灌注组。结论IPC可减轻CPB中缺血-再灌注心肌细胞的损伤,有利于术后早期心功能的恢复。     

含不同浓度乳化异氟醚的停跳液对大鼠离体心脏缺血再灌注损伤的影响

目的 探讨含不同浓度乳化异氟醚的停跳液对大鼠离体心脏缺血再灌注损伤的影响.方法 清洁级雄性成年SD大鼠,体重180～250 g,建立Langendorff离体心脏灌注模型,取模型制备成功的56个心脏随机分为7组(n=8):St.Thomas停跳液组(C组)和含不同浓度乳化异氟醚的停跳液组(E1组～E6组).K-H液平衡灌注20 min后,C组用4℃ St.Thomas停跳液20 ml使心脏停搏45 min,K-H 液再灌注60 min,E1组～E6组分别用含乳化异氟醚0.28、0.56、1.12、1.68、2.24和2.80 mmol/L的4℃St.Thomas停跳液20 ml使心脏停搏45 min,K-H液再灌注60 min.于平衡灌注末、再灌注20、40、60 min 时记录HR、左心室发展压(LVDP)、左心室舒张末压(LVEDP)和左心室压力最大上升速率(+dp/dtmax),并收集冠脉流出液1.5 ml,测定乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的活性和肌钙蛋白I(cTnI)浓度.于再灌注60 min时取心肌组织,计算心肌梗死面积.结果 与C组比较,E4组HR、LVDP、+dp/dtmax和SOD活性升高,LVEDP、LDH的活性和cTnI浓度降低,心肌梗死面积减小,E5组和E6组HR、LVDP、+dp/dtmax和SOD活性降低,LVEDP、LDH活性和cTnI浓度升高,心肌梗死面积增加(P<0.05),E1组～E3组上述指标差异无统计学意义(P>0.05).与E4组比较,其余含不同浓度乳化异氟醚的停跳液组HR、LVDP、+dpldt～和SOD活性降低,LVEDP、LDH活性和cTnI浓度升高,心肌梗死面积增加(P<0.05).结论 含1.68 mmol/L乳化异氟醚的停跳液可减轻大鼠离体心脏缺血再灌注损伤.     

常温不停跳心内直视手术冠脉血心肌酶、SOD、GHS及LPO的变化

目的 观察常温沁脏不停跳心内直视手术与冷停跳手术患者冠脉血心肌酶、超氧化物歧化酶（ＳＯＤ）、谷胱甘肽（ＧＳＨ）、脂质过氧化物（ＬＰＯ）的变化，明确不停跳手术对心肌保护作用。方法 ３６例心内直视手术患者随机分成不停跳与冷停跳组，每组１８例。不停跳组分别于体外循环前、体外循环１５分钟、体外循环停止时、机停后３０、６０分钟采血。冷停跳组分别于体外循环前、主动脉阻断时、主动脉开放时、开放后３０、６０分钟采     

Myocardial Performance After Cardiopulmonary Bypass and Cardioplegic Arrest: Impact of Na + /H + Exchanger Inhibition

This study was designed to determine if pretreatment with a sodium/hydrogen exchange inhibitor (EMD 96 785) improves myocardial performance and reduces myocardial edema after cardioplegic arrest (CPA) and cardiopulmonary bypass (CPB). Anesthetized canines ( n = 18) were instrumented with vascular catheters, myocardial ultrasonic crystals, and left ventricle (LV) micromanometer to measure preload recruitable stroke work (PRSW), + dP/dt max , and cardiac output. Serial myocardial tissue water content (MWC) was determined from sequential biopsy. After baseline measurements, hypothermic (28°C) cardiopulmonary bypass was initiated. CPA was maintained for 2 h, followed by reperfusion/rewarming and separation from CPB. PRSW and myocardial tissue water were measured at 30, 60, and 120 min after CPB. EMD 96 785 (3 mg/kg) was given 15 min prior to CPB. Controls received the same volume of saline vehicle. It was found that MWC increased from baseline in both EMD 96 785 and controls with CPB/CPA. PRSW decreased from baseline at 30 and 60 min post CPB/CPA in controls; PRSW did not decrease from baseline with EMD 96 785, and was statistically greater at 30 and 60 min post CPB/CPA compared to controls. Thus, Na + /H + exchanger inhibition with EMD 96 785 (3 mg/kg) pretreatment improves post-CPB/CPA myocardial performance without reducing myocardial edema. Na + /H + exchanger inhibition during cardiac procedures using CPB/CPA may be a useful adjunct to improve immediate post-CPB/CPA myocardial performance.     

Myocardial performance after cardiopulmonary bypass and cardioplegic arrest: impact of na+/h+ exchanger inhibition.

This study was designed to determine if pretreatment with a sodium/hydrogen exchange inhibitor (EMD 96 785) improves myocardial performance and reduces myocardial edema after cardioplegic arrest (CPA) and cardiopulmonary bypass (CPB). Anesthetized canines (n = 18) were instrumented with vascular catheters, myocardial ultrasonic crystals, and left ventricle (LV) micromanometer to measure preload recruitable stroke work (PRSW), +dP/dt(max), and cardiac output. Serial myocardial tissue water content (MWC) was determined from sequential biopsy. After baseline measurements, hypothermic (28 degrees C) cardiopulmonary bypass was initiated. CPA was maintained for 2 h, followed by reperfusion/rewarming and separation from CPB. PRSW and myocardial tissue water were measured at 30, 60, and 120 min after CPB. EMD 96 785 (3 mg/kg) was given 15 min prior to CPB. Controls received the same volume of saline vehicle. It was found that MWC increased from baseline in both EMD 96 785 and controls with CPB/CPA. PRSW decreased from baseline at 30 and 60 min post CPB/CPA in controls; PRSW did not decrease from baseline with EMD 96 785, and was statistically greater at 30 and 60 min post CPB/CPA compared to controls. Thus, Na(+)/H(+) exchanger inhibition with EMD 96 785 (3 mg/kg) pretreatment improves post-CPB/CPA myocardial performance without reducing myocardial edema. Na(+)/H(+) exchanger inhibition during cardiac procedures using CPB/CPA may be a useful adjunct to improve immediate post-CPB/CPA myocardial performance.     

吡那地尔超极化停搏对大鼠离体心脏缺血再灌注时p38MAPK表达的影响

目的 评价吡那地尔超极化停搏对大鼠离体心脏缺血再灌注时p38丝裂原活化蛋白激酶(p38MAPK)表达的影响.方法 成年雄性SD大鼠48只,体重250～300 g,采用随机数字表法,将大鼠随机分为6组(n=8):自然停搏组(A组)、St.Thomas组(B组)、吡那地尔超极化停搏组(C组)、5-羟葵酸(5-HD)组(D组)、HMR-1098组(E组)和5-HD+HMR-1098组(F组).采用Langendorff离体心脏灌注模型,K-H液平衡灌注15 min后,A组阻断主动脉,不予停搏液灌注,使其自然停搏;B组灌注St.Thomas停搏液;C组灌注吡那地尔超极化停搏液;D组、E组和F组K-H液平衡灌注10 min后,分别灌注含5-HD、HMR-1098、5-HD+ HMR-1098的K-H液5min,再灌注吡那地尔超级化停搏液.心脏停跳缺血60 min后,K-H液再灌注30 min.于平衡灌注15 min和再灌注20 min时记录冠脉流量(CF)、心率(HR)、左室发展压(LVDP)、左室收缩压(LVSP)和左室压力瞬时最大变化率(dp/dtmax);于再灌注30 min时取心肌组织,采用Western blot法测定心肌磷酸化p38MAPK和非磷酸化p38MAPK的表达.结果 与C组相比,A组、B组、D组、E组和F组再灌注20min时CF、HR、LVSP、LVDP及dp/dt/dymax降低,再灌注30 min时磷酸化p38MAPK表达下调,非磷酸化p38MAPK表达上调(P＜0.05);与E组相比,D组和F组再灌注20 min时CF、HR、LVSP、LVDP及dp/dtmax降低,再灌注30 min时磷酸化p38MAPK表达下调,非磷酸化p38MAPK表达上调(P＜0.05).结论 吡那地尔超极化停搏可改善大鼠离体缺血再灌注心脏功能,其机制与上调磷酸化p38MAPK表达,下调非磷酸化p38MAPK表达有关,而这种调控作用与线粒体ATP敏感性钾通道关系更密切.     

Comparison of myocardial protective effects between GIK solution and St. Thomas solution by use of canine isolated heart-lung preparations

The myocardial protection afforded by GIK solution, widely used as cardioplegic solution in this country, was compared with that provided by St. Thomas solution or oxygenated St. Thomas solution. Eighteen isolated heart-lung preparations of dogs were made and their hearts were subjected to 3 hours cold (4 degrees C) cardioplegic arrest. GIK group hearts (n = 6) received 20 ml/kg of GIK solution at the time of aortic cross-clamp perfused through the aortic root and were subsequently given 10 ml/kg of GIK solution every 30 minutes. St. Thomas group hearts (n = 6) and oxygenated St. Thomas group hearts (n = 6) were treated identically except that cardioplegic solution were St. Thomas solution or fully oxygenated one. Four hearts of GIK group showed ventricular fibrillation immediately after reperfusion that required DC countershock. Temporary A-V block was recognized in two hearts. In the other two groups, however, neither ventricular fibrillation nor A-V block was found. Heart rate, coronary flow, aortic flow and LVSW were measured before arrest and after 60 minutes of reperfusion (mean aortic pressure 70 mmHg, left atrial pressure 4 mmHg). Post reperfusion % recovery rates (post-reperfusion/before arrest) of heart rate, coronary flow, aortic flow and LVSW (mean value +/- standard deviation) were 93.4 +/- 10.32%, 104.6 +/- 24.91%, 18.8 +/- 8.54%, 32.6 +/- 6.12% respectively for GIK group, 81.4 +/- 6.50%, 125.9 +/- 15.23%, 35.4 +/- 9.91%, 56.3 +/- 12.90% for St. Thomas group and 83.1 +/- 8.40%, 121.6 +/- 16.92%, 47.0 +/- 7.89%, 69.1 +/- 9.71% for oxygenated St. Thomas group. St. Thomas and oxygenated St. Thomas groups revealed significantly (p less than 0.05, p less than 0.01 respectively) more excellent functional preservation than GIK group. Intramyocardial pH was also measured by use of glass needle pH electrode punctured into the anterior interventricular septum. Preischemic intramyocardial pH (at 37 degrees C) was 7.49 +/- 0.106 in GIK group, 7.48 +/- 0.113 in St. Thomas group and 7.43 +/- 0.114 in oxygenated St. Thomas group. During 3 hours of cardioplegic arrest, intramyocardial pH (at 4 degrees C) decreased to 6.84 +/- 0.101 in GIK group, 7.03 +/- 0.088 in St. Thomas group and 7.23 +/- 0.239 in oxygenated St. Thomas group, which was significantly higher than GIK group (p less than 0.01). Therefore oxygenated St. Thomas solution was found to maintain more favorable energy supply to ischemic myocardium. These results clearly evidenced that St. Thomas and oxygenated St. Thomas solutions would provide more effective myocardial protection during ischemic arrest than GIK solution.