冷血停搏液对法洛四联症婴幼儿心肌代谢的影响

目的：通过临床应用，评价冷血停搏液对未成熟心肌代谢的影响。方法：50例行择期法洛四联症根治术病儿随机分为2组，对照组用10℃改良St.Thomas 1停搏液（CCP），试验组用冷血停搏液（BCP），阻断升主动脉前，开放升主动脉1，3，10min分别由冠状静脉窦和动脉同时取血测定血气，电解质，乳酸，丙二醛（MDA）等含量。结果：再灌注后BCP组心肌氧提取率，乳酸摄取率恢复较快（P＜0．05），再灌注各时点两组均出现钾离子释放和MDA升高；再灌注后BCP组钙离子摄取较低（P＜0．05），结论：冷血停搏液对再灌注后的离子平衡，氧化谢，糖代谢恢复优于冷晶体停搏液。     

缺血预适应对体外循环心肌保护作用的实验研究

目的：比较单独应用冷停博液与缺血预适应及冷停博液联合应用对冠心病直视手术中的心肌保护作用。方法：１３只成年杂种犬随机分为对照组（６只）和实验组（７只），均在全麻下建立体外循环，实验组在阻断循环前实施５分钟－１０分钟方案的缺血预适 ，对照组只进行转机和冷停博液灌注，不进行缺血预适应方案。两组阻断循环后阻断冠状动脉前降支，建立冠脉梗阻模型，在开放主动脉交楹开前降支阻断带，模拟ＣＡＢＧ过程。结果：缺血预     

冠状动脉分支阻塞时冷停搏液顺灌加控制压力冠状静脉窦堵塞心肌保护的研究

实验犬在体外循环下，阻断升主动脉，使心脏缺血１２０’，同时阻断左前降支，顺行灌注冷停搏液，每２０分钟一次。实验分为：冠状静脉窦不加压组（对照组），加压２ｋＰａ组和加压４ｋＰａ组。开放升主动脉及左前降支后，辅助循环４０分钟，停机，不用正性心力药物，观察６０分钟。在同一心脏前负荷下，测量心排量（ＣＯ），与转流前ＣＯ对比，见ＣＯ恢复％在２ｋＰａ组及４ｋＰａ组均明显优于对照组（Ｐ＜０．０１）。实验结束时，左心室肌超微结构亦显示在２ｋＰａ组改变轻微，但在缺血前、后左心室肌ＡＴＰ及血清酶的改变，各组未见明显差异，本实验提示：在冠状动脉分支阻塞时，顺灌冷停搏液，同时以２ｋＰａ压力堵塞冠状静脉塞，可提高心肌保护作用，并对心肌无损伤害。     

缺血预适应对缺血脊髓保护作用的实验研究

目的：探讨缺血预适应对缺血脊髓的保护作用及其可能机制。方法：48只成年大耳白兔随机分为两组，每组24只，建立脊髓缺血模型。缺血预适应组（IPC组）采用腹主动脉阻断5min，开放15min的预适应方案后，再阻断40min后开放。对照组常规阻断腹主动脉40min后开放。分别于阻断前、阻断40min后、开放后2、8、24和72h，测定脑脊液超氧化物歧化酶（SOD）、脊髓脂质过氧化物酶（LPO）及脊髓组织含水量，并行双后肢神经功能评分。结果：IPC组各时相脑脊液SOD活性及神经功能评分显著优于对照组（P＜0．05），脊髓LPO含量及组织含水量明显低于对照组（P＜0．05）。结论：缺血预适应通过调动与增强脊髓组织内源性抗损害机制对缺血脊髓发挥保护作用。     

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。     

缺血预处理在心瓣膜置换术中对心肌保护的作用

目的研究单一周期的缺血预处理（IP）方法在心脏瓣膜手术中对心肌的保护作用。方法2002年8月至2006年4月85例慢性心瓣膜疾病患者在我院行心脏瓣膜手术，将其随机分为两组，IP组（n=47）：主动脉阻断前文行单次缺血2min开放3min的预处理方案，阻断主动脉后采用冷晶体心脏停搏液心肌保护方法；对照组（n=38）：仅采用冷晶体心脏停搏液心肌保护方法。观察两组术前、术后心肌型肌酸激酶同工酶（CK-MB）、肌钙蛋白I（cTnI）、心电图ST-T改变、室性心律失常及ICU临床指标。结果术后两组血清CK-MB和cTnI均较术前升高；IP组术后24、48和72h的CK-MB测量值，以及术后24和48h cTnI测量值均低于对照组（P〈0．05）。IP组术后使用抗心律失常药物的比率和持续时间明显低于对照组（P〈0．05），术后使用的正性肌力药物种类和ICU停留时间少于／短于对照组（P〈0．05）。结论IP和低温高钾晶体心脏停搏液灌注方法联合使用，可以增强心脏瓣膜手术中对心肌的保护效果，降低术后心肌酶、肌钙蛋白上升水平和术后室性心律失常程度，提高手术效果。     

常温体外循环下常温充氧晶体和氧合血停搏液持续灌注的心肌…

对比研究常温体外循环下常温充氧晶体和氧合血停搏液持续灌注对阻断升主动脉后犬心肌的保护效果，１５只犬随机分三组，每组５只，即低温体外循环冷搏液间断灌注组；常温体外循环常温氧合血停搏液持续灌注组；常温体外循环常温充氧晶掏搏液持续灌注组。观察了阻断升主动脉前心肌超微结构，腺苷酸含量（ＡＴＰ、ＡＤＰ、ＡＭＰ）、脂质过氧化物、水含量及血流动力学的变化。结果显示，温血组和温晶组在阻断升主动脉１５分钟、５０分钟     

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     

核转录因子κB对羊缺血预适应心肌细胞凋亡的影响

2003年1月至2004年3月,本研究对特异性核转录因子кB(NFκB)抑制剂脯氨酸二硫氨基甲酸酯(ProDTC)对缺血预适应(IPC)心脏保护效应的影响进行观察,并从细胞凋亡角度探讨NFκB在IPC中的作用。材料与方法1.动物分组:健康山羊18只(第二军医大学实验动物中心提供)均为雄性,体质量(29±3)kg,分为缺血再灌注(IR)组、IPC组及IPC+ProDTC组,每组6只。(1)IR组:建立体外循环,行体外循环1h后阻断上、下腔静脉,主动脉阻断后经主动脉根部灌注冷晶体停搏液使心脏停搏并间断顺灌行心肌保护,主动脉阻断60min后开放主动脉,心脏恢复血液灌注(再灌注)…     

30℃血停搏液心肌保护的临床与基础研究（158例报告）

自１９９１．６～１９９２．６采用３０℃血停搏液持续灌注进行心肌保护，对１５８名病人行心内直视手术。主动脉阻断１１～１５５ｍｉｎ，心脏自动复跳率８２．３％，手术成功率９８．７％，心肌生化及超微结构改变３０℃血停搏液均优于冷停搏液对照组（Ｐ＜０．０１）。且阻断时间越长，差异越显著。本方法是一种较理想的心肌保护方法。     

The effectiveness of ischemic preconditioning on myocardial protection and comparison with K(+) cardioplegia

The purpose of this study is to investigate the effects of ischemic preconditioning on myocardial protection and to compare this method to K(+) crystalloid cardioplegia. Langendorff perfused isolated working rat hearts were used in the following groups. After 20 min of stabilisation, 30 hearts were divided into three groups. In group I (control, n=10), hearts were arrested with cold (+4 degrees C) Krebs-Henseleit (K-H) solution, in group II (cardioplegia, n=10) hearts were arrested with cold K(+) cardioplegia solution, and in group III (preconditioning, n=10) hearts were subjected to 5 min normothermic ischemia followed by 5 min reperfusion then arrested with cold K-H solution. All hearts were subjected to 30 min of global ischemia (24 degrees C) and 40 min of reperfusion. Hemodynamic measurements were performed with a left ventricular latex balloon using a data acquisition system. Creatine kinase (CK-MB) washout and Troponin I (cTnI) levels were determined from the coronary effluents. There was no significant difference among the three groups in any of the parameters (hemodynamic and biochemical) measured at the end of stabilisation period. During reperfusion, functional recovery and coronary flow were significantly improved in K(+) cardioplegia and preconditioned groups compared with control group. CK-MB washout and cTnI levels were significantly lower in groups II and III compared with group I at the reperfusion. However no significant difference was observed between K(+) cardioplegia and preconditioned groups among biochemical and hemodynamic parameters and coronary flow at the post-ischemic period. In conclusion, ischemic preconditioning is as effective as K(+) cardioplegia on myocardial protection and recovery of myocardial function during reperfusion.     

A comparison between ischemic preconditioning,intermittent cross-clamp fibrillation and cold crystalloid cardioplegia for myocardial protection during coronary artery bypass graft surgery

The aim of this study was to compare ischemic preconditioning (IPC) with two established methods of myocardial protection, namely cold crystalloid cardioplegia and intermittent cross-clamp fibrillation (ICCF), in coronary artery bypass graft (CABG) surgery. This was a prospective randomised study. Thirty CABG patients were randomised to receive: (a) St Thomas' cardioplegia solution no. 2; (b) ICCF; or (c) IPC (two 3-min periods of ischemia with 2-min of reperfusion). Surgery was performed under standardised conditions by one surgeon (WBP). The primary endpoint was cardiac troponin T release during the first 72 h after surgery. Mean troponin T at 72 h was significantly lower in the IPC group (0.5 microg/l; p=0.05, ANOVA) compared with the cardioplegia and ICCF groups (2.1 and 1.3 microg/l respectively). This suggests that ischemic preconditioning is superior at limiting myocardial necrosis during CABG, but there is no difference between cold crystalloid cardioplegia and intermittent cross-clamp fibrillation.     

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。     

Relationship between hemodynamics and cardiac metabolism in the reperfusion period following hypothermic global ischemia

Ten mongrel dogs were subjected to hypothermic ischemic cardioplegia for two hours followed by 30 minutes of reperfusion to characterize the relationship between hemodynamic parameters during reperfusion and the recovery of high energy store of the post-ischemic left ventricular myocardium. Dogs were anesthetized with intravenous pentobarbital 30 mg/kg, and standard cardiopulmonary bypass was instituted with the flow rate of 80 ml/min/kg and perfusion pressure around 80 mmHg. Ischemic cardioplegia was obtained by cross-clamping of the aorta for 2 hours under 20°C of myocardial temperature. After termination of cardioplegia, the heart was rewarmed by the support of cardiopulmonary bypass with the flow rate of 80 ml/min/kg until the myocardial temperature reached 36 °C. Hemodynamic parameters were measured throughout the experiment and myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) were measured at the end of experiment. Correlation was significant between myocardial ATP and coronary blood flow and myocardial oxygen consumption. However, myocardial creatine phosphate correlated poorly to coronary blood flow, myocardial oxygen consumption and other hemodynamic parameters. These results indicate that the recovery of myocardial high energy store is partly related to coronary blood flow and myocardial oxygen consumption, but other parameters are probably involved in the process of early recovery of the myocardium from ischemic cardioplegia. This study was supported in part by a Grant from the Japan Heart Foundation for 1979.     

Adenosine-enhanced ischemic preconditioning provides enhanced cardioprotection in the aged heart

Background. Recently we have reported a novel myoprotective protocol “adenosine-enhanced ischemic preconditioning” (APC), which extends and amends the protection afforded by ischemic preconditioning (IPC) by both reducing myocardial infarct size and enhancing postischemic functional recovery in the mature rabbit heart. However, the efficacy of APC in the senescent myocardium was unknown.

Methods. The efficacy of APC was investigated in senescent rabbit hearts and compared with magnesium-supplemented potassium cardioplegia (K/Mg) and IPC. Global ischemia (GI) hearts were subjected to 30 minutes of global ischemia and 120 minutes of reperfusion. Ischemic preconditioning hearts received 5 minutes of global ischemia and 5 minutes of reperfusion before global ischemia. Magnesium-supplemented potassium cardioplegia hearts received cardioplegia just before global ischemia. Adenosine-enhanced ischemic preconditioning hearts received a bolus injection of adenosine in concert with IPC. To separate the effects of adenosine from that of APC, a control group (ADO) received a bolus injection of adenosine 10 minutes before global ischemia.

Results. Infarct size was significantly decreased to 18.9% ± 2.7% with IPC (p < 0.05 versus GI); 17.0% ± 1.0% with ADO (p < 0.05 versus GI); 7.7% ± 1.3% with K/Mg (p < 0.05 versus GI, IPC, and ADO); and 2.1% ± 0.6% with APC (p < 0.05 versus GI, IPC, ADO, and K/Mg; not significant versus control). Only APC and K/Mg significantly enhanced postischemic functional recovery (not significant versus control).

Conclusions. Adenosine-enhanced ischemic preconditioning provides similar protection to K/Mg cardioplegia, significantly enhancing postischemic functional recovery and decreasing infarct size in the senescent myocardium.     

Does hypothermia or hyperkalemia influence the preconditioning response?

Ischemic preconditioning (IPC) is a potent mode of myocardial protection, but not in all models of cold cardioplegia. The present study investigates possible effects of hypothermia and hyperkalemia on the preconditioning response. Langendorff-perfused rat hearts were preconditioned (2 min global ischemia and 5 min reperfusion) or control-perfused prior to 35 min normothermic, global ischemia (series 1, n = 17 in each group); 50 min normothermic cardioplegia (St. Thomas's II) (series 2, n = 10 in each); 75 min 23 degrees C, global ischemia (series 3, n = 7 in each); or 5 h 6-8 degrees C, global ischemia (series 4, n = 9 in each). Left ventricular developed (LVDP) and end-diastolic (LVEDP) pressures, coronary flow (CF), heart rate, incidence of severe reperfusion arrhythmias, and release of troponin T (TnT) were measured. IPC attenuated reduction of LVDP and CF, and increase of LVEDP during reperfusion in series 1-3. TnT release was reduced by IPC in series 3 only. IPC did not attenuate dysfunction after hypothermic ischemia (series 4). Neither hyperkalemia nor moderate hypothermia alone inhibited the preconditioning response, but IPC was not protective in deep hypothermia.     

卡托普利心脏停搏液对缺血再灌注心肌NOS活性和NO产生的影响

目的：探讨卡托普利心脏停搏液对缺血再灌注心肌保护作用的机制。方法：１２只绵羊,随机均分为对照组（Ｉ组）和卡托普利组（Ｉ组）。常规建立体外循环,心脏停搏６０分钟,再灌注３０分钟。Ｉ组采用仁济医院冷晶体停搏液,ＩＩ组在停搏液中加入卡托普利２３μｍｏｌ／Ｌ。观察冠状窦血中一氧化氮（ＮＯ）、肌酸磷酸激酶（ＣＰＫ）、环磷酸鸟苷（ｃＧＭＰ）、心肌丙二醛（ＭＤＡ）含量及心肌ＮＯ合酶（ＮＯＳ）同功酶活性的变化,监测心肌功能。结果：再灌注后Ｉ组心肌血ＮＯ、ＣＰＫ、ｃＧＭＰ、心肌ＭＤＡ均明显升高,Ｉ组低于Ｉ组（Ｐ＜０．０５或０．０１）。ＩＩ组再灌注后心肌原生型ＮＯ合酶（ｃＮＯＳ）活性明显高于Ｉ组,而诱导型ＮＯ合酶（ｉＮＯＳ）及总ＮＯＳ活性显著低于Ｉ组（Ｐ＜０．０１或０．００１）。两组再灌注后心肌功能均降低,Ｉ组较Ｉ组更为显著。再灌注后ＮＯ的变化与心肌ＭＤＡ和ＣＰＫ之间呈正相关（Ｐ＜０．００１和０．０１）。结论：缺血再灌注心肌损伤与过量ＮＯ产生有关,卡托普利通过调节ＮＯＳ同功酶活性,维持正常ＮＯ水平起到保护作用。     

Adenosine-enhanced ischemic preconditioning provides myocardial protection equal to that of cold blood cardioplegia

BACKGROUND: We recently described a novel myoprotective protocol-adenosine-enhanced ischemic preconditioning (APC)-that extends the protection of ischemic preconditioning (IPC) by both reducing myocardial infarct size and enhancing postischemic functional recovery in the isolated perfused heart. In the present report the efficacy of APC in the blood-perfused heart was investigated and compared with that of cold blood cardioplegia (CBC). METHODS: Cardiopulmonary bypass was instituted in 21 sheep hearts. The APC hearts (n = 6) received a bolus injection of adenosine through the aortic root at the immediate start of IPC (5 minutes of zero-flow global ischemia, followed by 5 minutes of reperfusion) before 30 minutes of global ischemia and 120 minutes of reperfusion. Nine other hearts received CBC. A control group (n = 6) received IPC only. RESULTS: Infarct size was significantly decreased (p<0.01) in the APC (3.0%+/-0.8%) and CBC (2.6%+/-0.2%) hearts compared with the IPC hearts (16.3%+/-1.6%). The preload recruitable stroke work relation, mean arterial pressure, and the time constant of pressure decay (tau) were significantly preserved (p<0.05) in APC and CBC hearts compared with IPC hearts. No significant differences were observed between APC and CBC hearts. CONCLUSIONS: Use of APC is as effective as CBC in significantly decreasing infarct size and enhancing post-ischemic functional recovery.     

Effects of ischemic preconditioning on myocardial protective on cardiac surgery: possibility of ischemic preconditioning and adenosine administration.

Subject: We evaluated the efficacy for concomitant use of ischemic preconditioning (IPC) and cardioplegic arrest with adenosine premedication on myocardial protection.Methods: Twenty-one pigs were divided into three groups: 1) control group, 2) IPC group which had IPC, 3) IPC+adenosine triphosphate (ATP) group which had an administration of 140 gamma of ATP (Adetphos, Kowa, Tokyo, Japan) during IPC. IPC was employed by 3 minutes of aortic cross clamping and 5 minutes of reperfusion. After cardioplegic arrest, the hemodynamical state was observed during 60 minutes of reperfusion. Serum adenosine, troponin-T, E-max, and Tau (the time constant of early diastolic left ventricular pressure decay) were compared. Results: Serum adenosine levels and at the end of IPC and 60 minutes reperfusion were significantly higher in the IPC and IPC+ATP groups than the control group. Comparison of the myocardial contractile force indicator E-max showed that the IPC and IPC+ATP groups showed significantly higher recovery rates of myocardial contractile force than the control group. Tau was the lowest in the IPC+ATP group than the other groups. In the histopathological study, the control group showed widely distributed hypercontraction bands and waving degeneration of myofibrils. On the other hand, the structure of myofibrils was well preserved in the IPC and IPC+ATP groups.Conclusions: The concomitant use of IPC enhanced the effect of a myocardial protective solution. However, the administration of adenosine during IPC did not show any further advantage than IPC along. (Ann Thorac Cardiovasc Surg 2003; 9: 307-13)     

缺血预处理对肢体缺血再灌注损伤的影响

目的　观察缺血预处理 (IPC)对肢体缺血再灌注损伤的影响。方法　选择 2 0例需充气止血带止血进行手术的患者 ,随机分为对照组 (n =10 )和IPC组 (n =10 )。IPC组患者术前应用 3次 5min循环缺血 ,间隔 5min再灌注预处理后在止血带下进行手术 ;对照组直接在止血带下进行手术。在肢体缺血前和再灌注 30min、90min、180min分别取静脉血检测血清肌酸磷酸激酶 (CPK)、谷草转氨酶(AST)、乳酸脱氢酶 (LDH)、丙二醛 (MDA)和过氧化物歧化酶 (SOD)水平。结果　随着肢体缺血再灌注时间的延长 ,血中CPK、AST、LDH、MDA含量逐渐升高 ,而SOD活性逐渐降低。IPC组在缺血前及再灌注同时间 ,血中CPK、AST、LDH、MDA含量低于对照组 (P <0 0 5 ,P <0 0 1) ;而SOD活性高于对照组 (P <0 0 5 ,P <0 0 1)。结论　IPC能有效地减轻肢体缺血再灌注损伤程度 ,减轻脂质过氧化反应 ,提高肢体缺血耐受性