1，6-二磷酸果糖停搏液心肌保护的对比研究

目的　观察外源性１ ,６二磷酸果糖（ Ｆ Ｄ Ｐ） 用于心脏停搏液,对心脏直视术期间心肌缺血的保护作用。方法　将１６ 例心脏瓣膜置换术患者随机分成 Ｓｔ ． ＴｈｏｍｓⅡ号停搏液组（ 对照组） 及 Ｆ Ｄ Ｐ停搏液组（ 实验组） 。观察两组不同停搏液灌注后病人心肌酶 Ｃ Ｐ Ｋ、心肌肌钙蛋白 Ｔ（ Ｃ Ｔｎ Ｔ） 的动态变化、术中心脏停搏情况、术后心脏复苏及血流动力学状况。结果　 Ｆ Ｄ Ｐ 停搏液组血清 Ｃ Ｐ Ｋ、 Ｃ Ｔｎ Ｔ 水平明显低于对照组。 Ｆ Ｄ Ｐ 加入停搏液能显著降低冠状静脉窦流出液 Ｍ Ｄ Ａ 的含量,心脏超微结构保存较好,术中心脏诱导停搏时间短,术后心脏复苏好,血流动力学稳定。结论　外源性 Ｆ Ｄ Ｐ 用于心脏停搏液,有明显的心肌保护效果。     

心得安对肥厚心肌的保护作用

目的 探讨心脏外科围手术期心得安预处理对肥厚心肌的保护作用. 方法 36只SD大鼠,采用随机数字表分为正常心肌组、肥厚心肌组和心得安组,腹主动脉缩窄制备大鼠心肌肥厚模型,采用离体工作心脏灌流模型,观察心脏自动复跳情况、心肌酶释放量的动态变化、心肌组织中丙二醛(MDA)含量和心肌超微结构改变. 结果 与肥厚心肌组比较,心得安组心脏自动复跳时间短,4种心肌酶释放量明显减少,上升幅度较缓,MDA含量低(P<0.01),心肌超微结构显示心肌细胞损伤较轻. 结论 术前用心得安预处理可缩短心脏手术后心脏自动复跳时间,减少肥厚心肌缺血-再灌注时心肌酶的释放,提高氧自由基清除能力,较好地保护心肌超微结构形态,对肥厚心肌具有保护作用.     

外源性磷酸肌酸对先天性心脏病矫治手术患儿心肌保护效果的Meta分析

目的：系统评价相关的随机对照研究以明确外源性磷酸肌酸对行先天性心脏病矫治手术患儿的心肌保护效果。方法：通过电子数据库检索所有研究外源性磷酸肌酸用于先天性心脏病矫治手术患儿的随机对照研究。由两位作者分别提取结果指标（包括术后心肌钙蛋白I水平、心脏自动复跳率、射血分数，正性肌力药物使用情况、机械通气时间），采用RevMan5．0软件进行Meta分析。结果：共纳入6项前瞻性随机对照研究，包括240例患者，其中磷酸肌酸组121例，对照组119例。与对照组相比．磷酸肌酸组患者术后心肌钙蛋白I水平降低（P〈0．01）．升主动脉开放后心脏自动复跳率增加（P〈0．01）．术后心脏射血分数增加（P〈0．05），正性肌力药物使用率降低（P〈0．01）、术后机械通气时间缩短（P〈0．01）。结论：外源性磷酸肌酸对行先天性心脏病矫治手术的患儿具有一定的心肌保护效果。     

心肌肌钙蛋白检测用于心脏瓣膜置换术中心肌保护措施的评价

目的应用心肌肌钙蛋白评价心脏瓣膜置换术中含血停搏液对心肌保护的优越性。方法将５０例心脏瓣膜置换术患者随机分为冷血心脏停搏液（ＢＣＰ）组和晶体心脏停搏液（ＣＣＰ）组,分别于转流前、主动脉阻断３０分钟和６０分钟、开放主动脉后２０分钟、术后１天、３天和７天采血测定心肌肌钙蛋白Ｔ亚单位（ｃＴｎＴ）及心肌酶谱。结果ｃＴｎＴ的敏感性优于心肌酶谱,ｃＴｎＴ的释放和心肌酶的渗出与心肌缺血时间成正比,主动脉阻断３０分钟以上者差异有显著性（Ｐ＜０．０１和Ｐ＜０．０５）,心脏自动复跳率和术后正性肌力药物的应用ＢＣＰ组均优于ＣＣＰ组（Ｐ＜０．０５）。结论ｃＴｎＴ可作为心脏外科心肌保护措施的常规检测指标,冷血心脏停搏液对长时间缺血心肌的保护作用优于晶体心脏停搏液     

吡那地尔介导超极化心脏停搏液对心肌的保护作用

目的：为了提高心脏停搏液的心肌保护作用，探讨含吡那地尔（pinacidil)超极化心脏停搏液对心肌的保护作用。方法：32只新西兰兔根据体外循环中使用不同的心脏停搏液分为对照组和实验组，对照组用St Thomas Ⅱ号心脏停搏液，实验组用含吡那地尔（50μmol/L）的心脏停搏液。两组又根据主动脉阻断后是否再灌注，分别分为两组（对照组A、对照组B、实验组A、实验组B），每组8只兔。对照组A和实验组A在主动脉阻断60分钟后结束实验；对照组B和实验组B于主动脉阻断60分钟、复滞30分钟结束实验。记录心脏电机械停搏时间，复跳时的心律失常情况，测定实验结束时各组心肌三磷酸腺苷（ATP）、总腺苷酸（TAN）、Ca^2 、丙二醛（MDA）含量，对照组B和实验组B血清心肌酶含量，并观察心肌超微结构变化。结果：4组心脏均迅速发生电机械停搏，对照组B、实验组B复跳时均发生心律失常3例，未发生严重心律失常；实验组A和实验组B的ATP、TAN分别高于对照组A和对照组B（P＜0．01），而Ca^2 和MDA分别显著低于对照组A和对照组B（P＜0．05），实验组B心肌酶的漏出量显著低于对照组B（P＜0．01）。实验组B超微结构损伤轻，优于对照组B。结论：含吡那地尔的心脏停搏液对心肌保护的作用优于高K^ 心脏停搏液。     

山茛菪碱防治双瓣膜替换病人心肌再灌注损伤的临床研究

风湿性联合瓣膜病变病人行双瓣膜替换术中更易遭受再灌注损伤。在实验研究基础上，作者将山茛菪碱（６５４－Ⅱ）加入心肌保护液中，以图改善这类病人术中心肌保护和探讨６５４－Ⅱ防治心肌再灌注损伤的机制。随机选择双瓣膜替换病人２０例，均分为常规心肌保护液对照组和常规心肌保护液加６５４－Ⅱ３０ｍｇ／Ｌ治疗组。１８例替换Ｍｅｔｒｏｎｉｃ－Ｈａｌｌ人工机械瓣，２例国产机械瓣。结果发现复跳前和复跳３０分钟，对照组冠状窦血乙酰胆碱均较用药组明显增加（Ｐ＜０．０５，０．００１）；相应时间Ｃａ￣（＋＋）、过氧化脂质含量也较用药组显著增加（Ｐ＜０．０５，０．０１）。手术结束后用药组病人心脏指数保持在较高水平（Ｐ＜０．０１），体循环阻力较对照组降低更明显（Ｐ＜０．０５，０．０１）。本研究提示，双瓣膜替换病人心肌保护液中使用６５４－Ⅱ可拮抗心脏迷走神经活动，明显增加心排量和降低全身血管阻力，较常规心肌保护措施更能有效地防治再灌注损伤。     

心肌肌钙蛋白I评价冷氧合血停跳和心脏不停跳的心肌保护效果

目的：探讨冷氧合血停跳和心脏不停跳的心肌保护效果。方法：50例心内直视手术病人随机分为冷氧合血停跳组（I组）和心脏不停跳组（Ⅱ组），每组25例，分别于术前，术后多个时点采取中心静脉血，测定血肌肌钙蛋白I（cTnI),CK,CK-MB，缺血前后观察心肌超微结构变化。结果：术前两组的cTnI,CK和CK－MB均在正常范围内，开放主动脉后1小时至术后24小时达峰值，其后缓慢下降，术后24小时心脏不停跳组CK水平明显低于冷氧合血组（P＜0．05），各时点cTnI,CK-MB水平两组间无显著性差异（P＞0．05），心肌超微结构于体外循环后两组间或与术前比较均无显著性差异（P＞0．05），结论：cTnI，心肌酶，心肌超微结构的动态变化提示冷氧合血停跳液与心脏不停跳的心肌保护效果相同。     

围CPB期血浆内源性洋地黄样活性物质的变化

观察１５例病人围ＣＰＢ期血浆内源性洋地黄样物质（ＥＤＬＳ）变化。结果：①ＥＤＬＳ麻醉后即下降，至主动脉开放前及心脏复跳后５分钟达最低值，心脏复跳后３０分钟回升近麻醉前水平；②ＣＶＰ、ＭＡＰ与ＥＤＬＳ变化趋势一致，ＥＤＬＳ与ＣＶＰ正相关；③主动脉阻断〈４５分钟、心脏自动复跳病人与主动脉阻断≥４５分钟、心脏除颤病人比较，主动脉开放前、心脏复跳后５分钟和３０分钟三个时点的ＥＤＬＳ均相应较低。提示：ＥＤＬ     

卡托普利抗心肌缺血再灌注损伤的实验研究

用兔体外循环心肌再灌注损伤模型，研究卡托普利（ｃａｐｔｏｐｒｉｌ，Ｃａｐ）的心肌保护作用。２０只兔随机均分为２组，建立体外循环后在主动脉阻断同时灌注４℃心脏停跳液，对照组为Ｓｔ．ＴｈｏｍａｓＩ号液，实验组在Ｓｔ．ＴｈｏｍａｓＩ号液中加入Ｃａｐ（０．５ｍｇ／ｋｇ）。心脏缺血９０分钟和再灌注６０分钟后结果显示，实验组心肌Ｃａ＋＋、丙二醛（ＭＤＡ）、心肌酶（ＬＤＨ，ＣＰＫ）较对照组显著降低，心肌超微结构损伤明显减轻。结论：Ｃａｐ对缺血再灌注心肌起到了良好的保护效果。     

心脏瓣膜置换术中防治心肌缺血／再灌注损伤的临床研究

在２７例心脏瓣膜置换术中观察了充氧停跳液和异搏定停跳液防治心肌缺血／再灌注损伤的效果，并以钾停跳液作为对照。分别在缺血前、再灌注前和再灌注后不同时期测定血清心肌酶（ＬＤＨ、ＣＰＫ、ＧＯＴ），心肌丙二醛（ＭＤＡ），观察心肌超微结构变化，并作线粒体比表面测定。结果显示充氧组和异搏定组再灌注后心肌酶释放量和心肌ＭＤＡ含量均明显低于对照组。心肌超微结构损伤轻，线粒体比表面无明显减小。提示充氧或异搏定钾停跳液能提供良好的心肌保护效果，减轻心肌再灌注损伤。     

外源性磷酸肌酸对未成熟心肌的保护作用

目的　观察外源性磷酸肌酸 (CP)对缺血未成熟心肌的保护作用。　方法　将 2 0例法洛四联症 (TOF)、室间隔缺损 (VSD)患者分为两组 ,对照组 :术中应用冷晶体心肌保护液 ;CP组 :应用 10 mmol/L CP强化冷晶体心肌保护液。观察两组患者心脏电生理指标、血流动力学恢复、正性肌力药物用量、心肌细胞超微结构和心肌酶浓度变化等。　结果　 CP组恢复窦性心律所需时间和正性肌力药物用量显著低于对照组 (P<0 .0 5 ) ;电子显微镜下 ,CP组超微结构保存较好 ,损伤比对照组小。　结论　 CP增强了冷晶体心肌保护液对未成熟心肌的保护作用。     

Biochemical changes induced in the myocardial cell during cardioplegic arrest supplemented with creatine phosphate

The purpose of this work was to evaluate the biochemical changes in the myocardial cell using cardioplegia supplemented with creatine phosphate (CP). Many previous studies have demonstrated the beneficial effect of CP on the ischemic myocardium and its mechanism of action has been assumed to be mainly extracellular. Based on the assumption that CP could also exert some influence on myocardial cellular metabolism, this investigation was carried out. Forty patients undergoing mitral valve replacement were divided into two groups: group 1 was treated with standard cardioplegic solution, and group 2 was treated with cardioplegic solution enriched with CP at a concentration of 10 mmol/L. Samples of papillary muscle, obtained from the removed valve, were studied by means of biochemical methods in order to assess the enzyme activities and the metabolites of the different biochemical pathways related to energy metabolism in the myocardial cell. One papillary muscle sample was used to determine enzyme activities spectrophotometrically; another was used to evaluate metabolite concentrations by spectrophotometric or spectrophotofluorimetric methods. The rate of spontaneous functional recovery after rewarming and weaning from cardiopulmonary bypass (CPB) also was evaluated. In group 2, the Vmax of enzymatic activities was significantly greater (hexokinase, malate dehydrogenase, glutamate dehydrogenase, total NADH cytochrome c reductase) and a better functional state of the heart was observed after CPB. On the basis of the clinical and biochemical data, it is concluded that the myocardium was better preserved when CP was added to the cardioplegic solution. Therefore, the results suggest a possible interaction of exogenous CP with cellular metabolism.     

The time course of myocardial high-energy phosphate degradation during potassium cardioplegic arrest

Myocardial high-energy phosphate and glucose-6-phosphate levels were determined in the in vivo pig heart model during ischemic arrest and reperfusion to determine the effectiveness of potassium cardioplegia in myocardial protection. Thirty-five pigs were divided into six experimental groups consisting of 2-hour normothermic arrest, 2-hour hypothemic arrest, 2-hour normothermic cardioplegic arrest, and 1-, 2-, and 3-hour hypothermic cardioplegic arrest. Myocardial biopsies from the left ventricle were obtained prior to arrest, every 30 minutes during the arrest interval, and at 30 and 60 minutes of reperfusion. The measurement of adenosine triphosphate and creatine phosphate showed that (1) cardioplegic arrest requires hypothermia to preserve high-energy phosphate levels in myocardial tissue; (2) hypothermia, while not completely protective alone, is more effective than potassium cardioplegia alone in providing myocardial preservation during 2-hour ischemic arrest; (3) the combination of potassium cardioplegia and hypothermia is additive in providing an effective means of maintaining myocardial high-energy phosphate stores during 1, 2, and 3 hours of ischemic arrest; (4) myocardial reperfusion does not allow a return to preischemic adenosine triphosphate (ATP) levels after 2 hours of arrest, except following hypothermic cardioplegia; and (5) extension of the duration of ischemic arrest to 3 hours using hypothermic cardioplegia prevents recovery of high-energy phosphate stores to preischemic levels during reperfusion. Optimal preservation can be achieved during 2 hours of ischemic arrest by using hypothermic potassium cardioplegia. The effects of myocardial reperfusion, however, prevent full ATP and creatine phosphate (CP) recovery following 3 hours of arrest. No other technique studied was as effective in providing myocardial preservation.     

Metabolic and functional effects of creatine phosphate in cardioplegic solution. Studies on rat hearts during and after normothermic ischemia

Creatine phosphate is a precursor molecule for ATP synthesis, even under ischemic conditions. We investigated its functional and metabolic effects when added to cardioplegic solution. Rat hearts were subjected to normothermic ischemia for 15 or 30 min and then freeze-clamped. During ischemia there was gradual reduction of high-energy phosphates, but the hearts with creatine phosphate supplement showed higher myocardial content of ATP and of the creatine compound. Other hearts, subjected to 20 min of ischemia, were reperfused with blood for 40 min. Creatine phosphate supplementation resulted in better left ventricular isovolumic work during spontaneous activity, but in paced activity (400 beats/min) no significant differences were seen. After reperfusion, supplemented hearts showed a tendency to higher levels of ATP and creatine phosphate. In all three groups the hearts with cardioplegic supplement had significantly increased myocardial content of pyruvate without proportional lactate increase. The results indicate that creatine phosphate may be an effective constituent in cardioplegic solution.     

Creatine phosphate: an additive myocardial protective and antiarrhythmic agent in cardioplegia

The potential for enhancing myocardial protection by adding high-energy phosphates to cardioplegic solutions was investigated in a rat heart model of cardiopulmonary bypass and ischemic arrest. Creatine phosphate (CP) was evaluated as an additive to the St. Thomas' Hospital cardioplegic solution. Dose-response studies (CP 0 to 50 mmol/L) revealed 10.0 mmol/L as the optimal concentration which improved recovery of aortic flow and cardiac output after a 40 minute period of normothermic (37 degrees C) ischemic arrest from 21.2% +/- 5.4% and 32.8% +/- 4.6% in the CP-free control group to 82.5% +/- 3.7% and 82.6% +/- 4.2% (p less than 0.001), respectively. Creatine kinase (CK) leakage was reduced by 68.7% (p less than 0.001) in the CP group. With hypothermic (20 degrees C) ischemia (240 minutes) and multidose (every 30 minutes) cardioplegia, recoveries of aortic flow and cardiac output were improved from 33.1% +/- 8.4% and 42.2% +/- 7.7% in the CP-free control group to 77.9% +/- 4.2% and 79.6% +/- 4.3% (p less than 0.001), respectively, in the drug group. In addition to improving function and decreasing CK release, CP reduced reperfusion arrhythmias, significantly decreasing the time between cross-clamp removal and return of regular rhythm and also completely obviating the need for electrical defibrillation. 51Chromium-ethylenediaminetetraacetic acid (51Cr-EDTA), an extracellular space marker, was used to study the disappearance of CP from the cardioplegic solution during its stasis in the heart. Upon reperfusion, two thirds of the infused dose appeared unchanged in the coronary effluent; the remainder was either degraded or accumulated by the myocardium. Despite its alleged inability to enter the myocardial cell, exogenous CP exerts potent protective and antiarrhythmic effects when added to the St. Thomas' Hospital cardioplegic solution. Although the mechanism of action remains to be elucidated, it may involve binding or uptake of the drug.     

含磷酸肌酸心脏停搏液对鼠供心的心肌保护作用

目的探讨含磷酸肌酸的心脏停搏液对离体心脏的保存效果，以延长供体心脏缺血的保存时间，提高心脏移植的效果。方法将20只Wistar大鼠随机分成两组，对照组（n=10）：使用冷晶体St．ThomasⅡ心脏停搏液灌注保护供心；实验组（n-10）：灌注含磷酸肌酸钠（2．5g／L）的冷晶体St．ThomasⅡ心脏停搏液保护供心。鼠心于低温保存4h后取心肌组织，测定心肌组织中三磷酸腺苷（ATP）含量和超氧化物歧化酶（SOD）活性。在光学显微镜和电子显微镜下观察心肌组织结构变化及线粒体水肿情况。结果供心冷藏保存4h后，实验组心肌组织中ATP含量明显高于对照组（2．75±0．99μmol／mg vs．1．77±0．86μmol／mg，P〈0．05）；SOD活性明显高于对照组（49．6±2．52U／mg vs．45．27±2．21U／mg，P〈0．05）。电子显微镜下观察：对照组心肌细胞核固缩，核膜内染色质凝聚、溶解，线粒体嵴间隙消失，间质血管内皮坏死；实验组心肌细胞核位于中心区，肌节各带结构清晰，肌质网扩张，闰盘各带连接结构清晰。结论含磷酸肌酸的心脏停搏液能明显增强供心的心肌保护作用。     

大剂量磷酸肌酸钠预先给药对心脏瓣膜置换术患者心肌缺血再灌注损伤的影响

目的 探讨大剂量磷酸肌酸钠预先给药对心脏瓣膜置换术患者心肌缺血再灌注损伤的影响.方法 择期拟行二尖瓣-主动脉瓣置换术患者246例,年龄42～71岁,体重45～80 kg,随机分为2组:对照组(NS组,n=122)和磷酸肌酸钠预先给药组(CP组,n=124).CP组切皮时开始中心静脉输注磷酸肌酸钠10g(溶于100ml生理盐水),输注时间60 min,NS组静脉输注等容量生理盐水,分别于麻醉前、术后第1天和第5天采集颈内静脉血样,检测血清磷酸肌酸激酶、乳酸脱氢酶、肌酸激酶同工酶的活性,测定心肌肌钙蛋白I浓度,观察心律失常、心肌梗塞的发生情况及自动复跳情况,记录使用正性肌力药多巴胺(≥5 μg·kg-1·min-1)和肾上腺素的患者例数及左室射血分数.结果 与NS组比较,CP组术后第1天和第5天血清磷酸肌酸激酶、乳酸脱氢酶、肌酸激酶同工酶的活性及心肌肌钙蛋白I浓度降低,使用多巴胺和肾上腺素的患者例数减少,术后心律失常和心肌梗塞的发生率降低,自动复跳率及左室射血分数升高(P<0.05).结论 大剂量磷酸肌酸钠(10 g)预先给药可减轻二尖瓣-主动脉瓣置换术患者的心肌缺血再灌注损伤,改善心脏功能.     

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     

Oxygen requirements of the isolated rat heart during hypothermic cardioplegia. Effect of oxygenation on metabolic and functional recovery after five hours of arrest

Previous studies from this laboratory demonstrated that the use of an oxygenated cardioplegic solution in the hypothermic arrested rat heart resulted in improved preservation of high-energy phosphate stores (adenosine triphosphate and creatine phosphate), mechanical recovery during reperfusion, and preservation of myocardial ultrastructure. In the current study the effect of cardioplegic solutions oxygenated with 30%, 60%, and 95% oxygen was evaluated in the isolated rat heart with reference to the maintenance of adenosine triphosphate, creatine phosphate, oxygen consumption, functional recovery, and mitochondrial oxidative phosphorylation in vitro. Results indicate that the hearts receiving cardioplegic solutions supplemented with 95% oxygen and 5% carbon dioxide maintained adenosine triphosphate and creatine phosphate at control values for at least 5 hours. The oxygen consumption during elective cardiac arrest, mechanical performance during reperfusion, and in vitro mitochondrial oxygen uptake and phosphorylation rate were highest in the hearts receiving cardioplegic solutions supplemented with 95% oxygen when compared to solutions with 30% and 60% oxygen. Addition of glucose and insulin to the cardioplegic solution (95% oxygen) increased the adenosine triphosphate levels but failed to improve function after reperfusion. Although myocardial adenosine triphosphate and creatine phosphate were well preserved by the oxygenated cardioplegic solution, there was a discrepancy between the adenosine triphosphate levels at the end of the arrest period, which represents the potential for mechanical function, and the actual function of the hearts after 5 hours.     

Creatine phosphate (Neoton) as an additive to St. Thomas' Hospital cardioplegic solution (Plegisol). Results of a clinical study

Experimentally, creatine phosphate (CP) added to St. Thomas' Hospital cardioplegic solution (STH) improved post-ischaemic recovery of cardiac function in the rat heart. We investigated the effect of adding CP (10.0 mmol/l) to STH. Fifty open-heart surgery patients were randomized into control (STH) and treated (STH + CP) groups (25 per group). Patients underwent (a) monitoring for peri- and postoperative arrhythmias (48-h Holter monitoring). (b) quantitative birefringence assessment of intraoperative myocardial protection in left and right ventricular biopsies sampled at start of bypass (pre-isch.), end of bypass (end-isch.) and after 10 min reperfusion (post-isch.), and (c) measurement of serum creatine kinase-MB isozyme (CK-MB) values for up to 4 days postoperatively; results were assessed with respect to (d) haemodynamics and postoperative clinical outcome. Inotropic support (adrenaline) was required in three patients (12%) from each group; no patient died. All patients required defibrillation, and the number of direct current shocks required for sinus rhythm was the same in each group. The occurrence and incidence of reperfusion-induced arrhythmias were the same in both groups. Serum CK and CK-MB values were similar throughout the sampling period in both groups of patients; one patient in the control group had raised CK-MB levels postoperatively, but perioperative infarction was not indicated by the electrocardiogram.(ABSTRACT TRUNCATED AT 250 WORDS)