心肌肌钙蛋白检测用于心脏瓣膜置换术中心肌保护措施？…

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组和晶体心脏停搏液组,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亚韵及心肌酶谱。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的时间成正比,主动脉阻断３０分钟以上者差异有显著性,心     

光量子冷血停搏液的心肌保护作用

目的 探讨光量子冷血停搏液的心肌保护效果。方法 建立离体兔心工作模型，将实验动物分为冷晶体停搏液组、冷血停搏液组、光量子冷血停搏液组和温血停搏液组，每组８只。心脏停搏３０分钟，复灌３０分钟。结果 复温复灌１０分钟及３０分钟时，光量子冷血组的冠脉流出量、心肌含水量、心肌内ＡＴＰ和磷酸肌酸（ＣＰ）含量的变化均明显优于冷晶体组和冷血组（Ｐ〈０．０５）。结论 光量子冷血停搏液能够改善心肌本身循环，增加氧的     

温血诱导心脏停搏及终末温血灌注在婴幼 儿心内直视术中的应用研究

目的探讨温血诱导心脏停搏及终末温血灌注技术在婴幼儿先天性心脏病（ＣＨＤ）手术中对心肌的保护作用。方法将４０例＜３岁ＣＨＤ患儿随机分成２组：温血诱导心脏停搏＋终末温血灌注组（温血组）;冷晶体液心脏停搏组（冷晶体组）。２组主动脉阻断时间无明显差异;体外循环前、后分别抽血测定乳酸脱氢酶（ＬＤＨ）、肌酸激酶（ＣＫ）、肌钙蛋白Ｔ（ＴｎＴ）;电子显微镜观察两组缺血后心肌超微结构。结果发现冷晶体组ＬＤＨ（１９７．９±７３．６Ｕ／Ｌ）,ＣＫ（１０７．６±５０．６Ｕ／Ｌ）,ＴｎＴ（８．９±４．０μｇ／Ｌ）升高值均高于温血组（８５．２±４７．７Ｕ／Ｌ,５５．８±３５．９Ｕ／Ｌ和３．３±２．４μｇ／Ｌ,Ｐ＜０．０５）,电子显微镜观察缺血后超微结构温血组优于冷晶体组。结论温血诱导心脏停搏及终末温血灌注技术对婴幼儿心肌保护作用有利     

腺苷预处理对体外循环术后心肌肌钙蛋白变化的影响

目的 探讨腺苷预处理对心脏直视手术的心肌保护效果。方法 ３０例择期心瓣膜置换术患者随机分成实验组和对照组，每组１５例。实验组在术前行腺苷预处理。分别于转流前、主动脉阻断３０分钟和６０分钟、主动脉开放后３０分钟及术后２４小时采血测定心肌肌钙蛋白Ｔ（ｃＴｎＴ）、心肌酶谱和丙二醛。结果 腺苷预处理ｃＴｎＴ和心肌酶外漏明显减少，丙二醛生成减少。结论 腺苷预处理能减轻心肌肌缺血再灌注损伤。     

温血灌注与冷晶体心脏停搏液灌注对心肌酶学的影响

目的比较温氧合血连续灌注与冷晶体心脏停搏液间断灌注心肌酶学变化,探索更有效的心肌保护方法。方法将阻断时间在６０分钟以上１６例患者随机分为温血灌注组（Ａ组）和冷晶体灌注组（Ｂ组）,每组８人。分别于主动脉阻断前和主动脉阻断６０分钟后取部分心肌组织测定其超氧化物歧化酶（ＳＯＤ）和脂质过氧化物（ＬＰＯ）并进行对比分析。结果阻断前和阻断后２组ＳＯＤ和ＬＰＯ含量无差异,阻断后Ｂ组ＳＯＤ含量比阻断前显著降低（Ｐ＜０．０１）;而阻断后ＬＰＯ含量明显增高（Ｐ＜０．０１）。结论温血连续灌注能有效减轻心肌缺血与再灌注损伤,满足心肌需氧代谢,保持停搏心肌抗氧化系统稳定     

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。     

氨基酸对未成熟心肌保护作用的实验研究

研究天门冬氨酸或（和）谷氨酸强化血停搏液对未成熟心肌的保护效果。将２４只出生３～４周新西兰幼兔随机均分成４组：Ｉ组为冷血停搏液组，Ｉ组天门冬氨酸（２０ｍｍｏｌ／Ｌ）强化组，ＩＩ组谷氨酸（２０ｍｍｏｌ／Ｌ）强化组，ＩＶ组谷氨酸加天门冬氨酸（各２０ｍｍｏｌ／Ｌ）强化组。结果表明，心功能指标心输出量（ＣＯ）恢复百分率ＩＶ组、Ｉ组明显少于Ｉ组（Ｐ＜０．０１）；左室收缩压（ＬＶＳＰ）恢复百分率Ｉ、ＩＩ、ＩＶ组明显少于Ｉ组（Ｐ＜０．０１）；左室舒张压（ＬＶＤＰ）及左室压力微分（ｄｐ／ｄｔ）恢复百分率Ｉ、ＩＩ、ＩＶ组优于Ｉ组（Ｐ＜０．０５）。乳酸脱氢酶（ＬＤＨ）和磷酸肌酶（ＣＫ）漏出量（Ｕ／Ｌ）中，ＬＤＨ漏出量Ｉ组优于Ｉ组（Ｐ＜０．０５），ＩＩ、ＩＶ组明显优于Ｉ组（Ｐ＜０．０１）；ＣＫ漏出量ＩＩ、ＩＶ组明显优于Ｉ组（Ｐ＜０．０１）。Ｉ、ＩＩ、ＩＶ组心肌含水量（％）明显优于Ｉ组（Ｐ＜０．０１）。Ｉ、ＩＩ、ＩＶ组心肌结构保护明显优于Ｉ组。结论：谷氨酸或（和）天门冬氨酸强化血停搏液能明显增强对未成熟心肌的保护作用。氨基酸强化组间之所以差别不显著可能与模型有关     

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。     

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。     

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。     

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。     

Effects of L-arginine cardioplegia on myocardium

Infusion of L-arginine (a precursor of nitric oxide, NO) in cardioplegia was examined to test its effect on metabolism of myocardium after myocardial ischemia and reperfusion (IR). Twenty-eight patients undergoing valve replacement were involved and randomly divided into two groups: the control group (crystalloid cardioplegia) and the experimental group (crystalloid cardioplegia + L-arginine). Blood samples were taken both before aortic clamping and after aortic unclamping from right radial artery to measure the concentrations of NO2-/NO3-, lactic acid (LA), malondialdehyde (MDA), superoxide dismutase (SOD), and xanthine oxidase (XOD). In the control group, the NO2-/NO3- level decreased at aortic unclamping, and 30 min later, it decreased significantly as compared with that before aortic clamping (p < .05). In the experimental group, it increased at aortic unclamping (p < .05), and 60 min later, increased to the peak. Five, fifteen, and thirty min after aortic unclamping, the concentrations of LA and MDA in the experimental group were lower than those in the control group (p < .05). Thirty and sixty min after aortic unclamping, the concentrations of SOD remained higher in the experimental group than those in the control group (p < .05). There was no difference between groups in the concentrations of XOD. The addition of L-arginine to the cardioplegia can protect the myocardium from injury by releasing nitric oxide.     

Low-dose histidine-tryptophan-ketoglutarate solution for myocardial protection

The effect of histidine-tryptophan-ketoglutarate (HTK) solution for myocardial protection has been shown in experimental and clinical studies using long ischemic times and high dosages. In our study we compared myocardial protection in isolated coronary bypass with a short period of ischemia using low dosage HTK and cold crystalloid cardioplegia. Each group contained 21 coronary artery disease patients. Cardioplegic solutions were administered antegrade in 10 to 15 mL/kg in one shot. This dosage of HTK was lower than that mentioned in the literature. We measured malondialdehyde, lactate, creatine kinase, creatine kinase-MB, and troponin-I levels. Aortic clamping time in the HTK group 33.9 +/- 8.2 minutes, versus 36.2 +/- 11.3 minutes in the crystalloid cardioplegia group (P > .05). Levels of creatine kinase and malondialdehyde were lower in HTK group at 24 hours and 2 minutes, respectively. Lactate levels were lower in the crystalloid cardioplegia group at 2 minutes in the coronary sinus serum sample, but there were no statistically differences among ischemic serum markers in both groups. Only intervals between aortic clamping and cardiac arrest were statistically meaningful (HTK 63.3 +/- 14.7 seconds versus crystalloid cardioplegia 53.6 +/- 15.6 seconds, P = .044). Our study shows that use of low-dose HTK for short clamping time operations is as successful for myocardial protection as crystalloid cardioplegia. Longer times for fibrillation can be explained with the low levels of potassium in HTK solution, but this length did not cause a biochemical or clinical difference.     

Regional myocardial perfusion of cardioplegic solutions

We compared the regional myocardial perfusion of blood cardioplegic solution (BCP) and crystalloid cardioplegic solution (CCP) in 14 mongrel dogs. Cardiopulmonary bypass was established at 28 degrees C, and a hydraulic occluder was placed around the proximal left anterior descending (LAD) coronary artery. In group 1 (N = 7) collateral coronary arteries were ligated; in group 2 (N = 7) collateral coronary arteries were left in situ. After the aorta was clamped, BCP and CCP were alternately perfused at 200 ml/min. The occluder was inflated to produce moderate, severe, and critical LAD stenosis, and regional perfusion was measured by xenon-133 washout with the Silicon Avalanche Radiation Detector. BCP infusion produced a consistently higher aortic pressure, but CCP flow was better than BCP flow under all conditions, particularly without coronary collaterals (p less than .05). Regional myocardial perfusion of CCP is superior to BCP.     

Protection of the myocardium during prolonged surgery of the heart valves]

The comparative analysis of the effectiveness of the use of blood and crystalloid cardioplegia in valve prosthetics with prolonged clamping of the aorta was carried out. The use of blood cardioplegia is preferable, especially in patients with low functional myocardial reserve.     

Terminal warm blood cardioplegia improves the recovery of myocardial electrical activity. A retrospective and comparative study.

OBJECTIVE: The effect of terminal warm blood cardioplegia was analyzed in 191 patients undergoing either coronary artery bypass grafting (CABG) or prosthetic heart valve replacement between Jan. 1990 and Dec. 1995. METHODS: Patients were subdivided into 3 historical cohorts based on the method of myocardial protection: Group A (n = 106), multidose cold crystalloid glucose-potassium cardioplegia, alone; Group B (n = 37), cold crystalloid glucose-potassium cardioplegia plus terminal warm blood cardioplegia, Group C (n = 48), cardioplegia induction with cold crystalloid glucose-potassium cardioplegia, maintenance with multidose cold blood cardioplegia, and terminal warm blood cardioplegia. RESULTS: Of patients undergoing CABG, 5.6% of group A, 70.4% of group B, and 86.7% of group C spontaneously resumed sinus rhythm after aortic declamping, as did 9.1% of group A, 60.0% of group B, and 55.6% of group C of patients undergoing prosthetic heart valve replacement. The incidence of spontaneous recovery was significantly better in groups B and C than in group A (p < 0.05). Over 90% of patients without terminal warm blood cardioplegia developed ventricular fibrillation or tachycardia requiring electrical cardioversion (p < 0.05). Postoperatively, patients without terminal warm blood cardioplegia required temporary epicardial pacing more frequently than those with terminal warm blood cardioplegia (p < 0.05). In patients undergoing prosthetic heart valve replacement, groups B and C, the incidence of postoperative atrial fibrillation was significantly lower than in group A. CONCLUSION: Terminal warm blood cardioplegia thus promoted better postoperative electrophysiological cardiac recovery.     

The superiority of continuous cold blood cardioplegia in the metabolic protection of the hypertrophied human heart

The effects of sanguineous and asanguineous cardioplegia on the generation of myocardial acid in the hypertrophied human heart during aortic clamping and reflow were elucidated by continuous intraoperative monitoring of myocardial pH in 42 patients undergoing valve replacement, with or without coronary bypass. The patients were divided into three groups: Group I (n = 14) received intermittent crystalloid cardioplegia; group II (n = 14) received intermittent blood cardioplegia; and group III (n = 14) received continuous blood cardioplegia. The groups were matched according to six previously elucidated determinants of myocardial acidosis. Measurements were made of myocardial pH, hydrogen ion concentration ([H+]), and the difference in pH units between myocardial pH and the pH of neutrality of water at the corresponding temperature (delta pHn). Throughout aortic clamping, myocardial pH in groups I and II fell significantly by 0.46 +/- 0.08 and 0.15 +/- 0.07 units, respectively (p less than 0.001) between the groups). In contrast, myocardial pH remained statistically unchanged throughout aortic clamping in group III (p less than 0.001 compared to groups I and II). Similar relationships were observed in [H+] and delta pHn during aortic clamping. During the early reflow, myocardial acidosis was observed in all three groups and delta pHn in group III increased from -0.26 +/- 0.10 at the end of aortic clamping to -0.57 +/- 0.07 during reperfusion (p less than 0.03). Patients in groups II and III required significantly less inotropic and mechanical cardiac support than patients in group I (p = 0.017). Hence, although continuous blood cardioplegia does not completely prevent acid accumulation during reflow, it provides better metabolic protection of the hypertrophied human heart than either intermittent crystalloid or intermittent blood cardioplegia.     

体外循环心脏手术相关因素致肌钙蛋白T变化的研究

目的 观察体外循环心脏手术相关因素致心肌细胞的损害程度,通过心肌肌钙蛋白Ｔ变化找出其相对规律及数据,为临床提供心肌保护措施及理论根据。方法 随机选择３７例心脏手术,其中心脏瓣膜替换术１５例,先天性心脏病１５例,冠状动脉搭桥７例,于手术前、停机时、术后５ｈ、术后第１天、术后第２天抽 血检测肌钙蛋白Ｔ浓度的变化经统计学处理,ｑ检验进行对比研究。结果 （１）主动脉阻断时间〉６０ｍｉｎ组术后５小时肌钙蛋白     

Improved profile of bad phosphorylation and caspase 3 activation after blood versus crystalloid cardioplegia

BACKGROUND: Expression of Bcl-2 family proteins and activation of terminal caspase 3 are important for ischemia-reperfusion-induced apoptosis. Bad and Bax are pro-apoptotic proteins, whereas, phosphorylation of Bad inhibits its binding to and inactivation of anti-apoptotic Bcl-2. Thus, decreases in phospho-Bad would be proapoptotic. We investigated if blood (BCP) or crystalloid cardioplegia (CCP) differentially affects apoptosis gene-related proteins. METHODS: Rabbit hearts were perfused with Krebs-Henseleit buffer (KHB) on a Langendorff apparatus. Control hearts (n = 6) were perfused for 90 minutes without cardioplegic ischemia. In the other two groups, hearts were arrested for 30 minutes (37 degrees C) with BCP (n = 6) or with CCP (n = 6) administered continuously (1.5 mL/min). The hearts were reperfused for 30 minutes with KHB. Left ventricle (LV) performance was measured before cardioplegic arrest and at 30 minutes of reperfusion. In vitro relaxation responses of precontracted microvessels (100-180 microm) were obtained in a pressurized no-flow state. Total and activated or phosphorylated caspase 3, Bcl-2, Bad, and Bax were measured by quantitative immunoblotting using specific antibodies. RESULTS: Blood cardioplegia significantly improved the recovery of LV developed pressure compared to CCP (p < 0.05). The endothelium-dependent relaxation in response to adenosine 5'-diphosphate was greater after BCP than after CCP (59.9 +/- 4% vs 26.9 +/- 6%, respectively; p < 0.05). There were no differences in total protein levels of caspase 3, Bcl-2, Bad, and Bax between the groups. Both BCP and CCP increased caspase 3 activity as compared with controls, but CCP caused more activation of caspase 3 than BCP (6.2 +/- 0.7 fold vs 3.1 +/- 0.4, p < 0.05). Both BCP and CCP induced phosphorylation of Bad at Ser(112), but BCP caused greater phosphorylation of Bad (3.5 +/- 0.2 fold vs 2.0 +/- 0.12 fold, respectively, p < 0.05) than CCP. CONCLUSIONS: Blood cardioplegia is superior to CCP in inhibiting the activation of caspase 3 and in increasing phospho-Bad. These actions of BCP were associated with improved LV function and endothelium-dependent relaxation of coronary microvessels. These results may provide molecular mechanisms by which to improve myocardial protection during cardiac surgery.