常温氧合血与冷晶体心脏停搏液心肌保护对比研究

目的　为了探索较好的心肌保护方法,对持续常温氧合血心脏停搏液和间断冷晶体心脏停搏液灌注两种方法的心肌保护作用进行了对比研究。　方法　心瓣膜直视术患者３３ 例,随机分为常温氧合血心脏停搏液组（ Ｗ Ｂ Ｃ组）和冷晶体心脏停搏液组（ Ｃ Ｃ Ｃ组）。观察两组术后主要并发症、起搏器的使用情况,测定主要心肌酶。肌酸激酶、肌酸激酶同工酶、乳酸脱氢酶同工酶的释放,丙二醛、超氧化物歧化酶、三磷酸腺苷的含量以及能量储备值,观察心肌超微结构的变化。　结果　术后低心排血量综合征、室性心律失常发生例数、起搏器使用率和肌酸激酶同工酶的释放, Ｃ Ｃ Ｃ组均较 Ｗ Ｂ Ｃ组多;丙二醛释放和心内源性超氧化物歧化酶消耗, Ｗ Ｂ Ｃ组较 Ｃ Ｃ Ｃ组减少;能量保存 Ｗ Ｂ Ｃ组较 Ｃ Ｃ Ｃ组多;心肌细胞内线粒体损伤以 Ｃ Ｃ Ｃ组为重。　结论　常温氧合血心脏停搏液持续灌注在心肌保护方面较冷晶体心脏停搏液间断灌注具有明显的优越性,是一种较好的心肌保护方法。     

温氧合血停搏液诱导停搏及复苏再灌对心肌保护的作用

为观察不同灌注方法改善心肌保护的效果，用杂种犬２１只，随机均分为３组：Ｉ、Ｉ组分别用冷晶体、冷氧合血停搏液间灌，ＩＩ组在Ｉ组基础上加用温氧合血停搏液诱导停搏及复苏再灌。于体外循环下心肌缺血９０分钟再灌注３０分钟期间，观察心脏电机械活动、转流前后左心功能、心肌ＣＰＫ释放量及摄氧量、心肌含水量及超微结构变化。结果显示：Ｉ、ＩＩ组复苏后血流动力学的稳定性、左心功能恢复优于Ｉ组，ＣＰＫ释放量、心肌含水量及超微结构损害程度明显低于Ｉ组。ＩＩ组心肌停搏及复苏极少出现室颤、自动复跳率高、心肌摄氧量高于Ｉ组；再灌注３０分钟时，心肌ＣＰＫ释放量明显低于Ｉ组，心肌水肿及超微结构损伤较Ｉ组略轻。表明冷氧合血停搏液间灌法具有明显减轻心肌缺血和再灌注损伤的作用，而温氧合血停搏液诱导停搏及复苏再灌的心肌保护效果更佳。     

体外循环常温氧合血连灌与低温冷晶体液间灌心停搏法的对比研究

自１９９１年１月至１９９２年６月，将１２０例病人均分为常温氧合血连续灌注组与低温冷晶体液间断灌注组。研究结果显示：常温组心室纤颤率、手术死亡率及心功能改善率均明显优于低温组；低温组心肌超微结构损害严重，常温组则无明显损害。     

温血和冷晶体停搏液的心肌保护效果比较

１９９１年至１９９６年，我们采用温血停搏液心肌保护方法行各种心脏瓣膜替换术１７６例，与同期采用传统冷晶体停搏液行瓣膜替换术的１３４例病人比较，疗效好，现报告如下。资料和方法　３１０例行心脏瓣膜替换术病人分为温血停搏液组（简称ＣＷＢＣ组）１７６例和冷晶体停搏液组（简称ＣＣＣ组）１３４例。ＣＷＢＣ组男８４例，女９２例；心功能ＩＩ、Ⅲ、Ⅳ级者分别为１４例（８％）、８８例（５０％）、７４例（４２％）；伴房颤者１５２例（占８６％）；行二尖瓣替换术１１６例、主动脉瓣替换术２９例、双瓣替换术３１例。ＣＣＣ组…     

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     

温血和冷晶体停搏液应用于换瓣病人心肌保护的对比研究

我院近来观察了温血和冷晶体心脏停搏液对166例心脏瓣膜置换手术的心肌保护作用，现报告如下。     

冷晶体停搏液间断灌注和温血停搏液连续灌注法对心脏直视手术患者心肌的保护作用

本研究通过观察心脏直视手术患者心肌肌钙蛋白I(cTnI)及心肌超微结构的变化,评价冷晶体停搏液间断灌注和温血停搏液连续灌注法对心肌的保护效果。资料和方法选择心脏瓣膜置换术患者20例,随机分为温血组和冷晶组,每组10例;灌注方法:胸骨正中劈开建立体外循环后,冷晶组:肛温降至28℃～30℃时用改良St.Thomas冷晶体停     

温血停搏液诱导与末次灌注心肌保护作用研究

离体鼠心工作模型，采用温血停搏液诱导与末次灌注结合冷晶体停搏液及局部低温行心肌保护研究，并与单纯冷晶体停搏液及局部低温进行了比较。结果表明，温血停搏液诱导与末次灌注能增加心肌ＡＴＰ的储备，促进心功能恢复，心肌酶释放少，超微结构改变轻，心肌保护效果优于单纯采用冷晶体停搏液组。     

顺行灌注冷晶体停搏液及温血停搏液对心肌的保护作用

目的研究冷晶体及温血停搏液对心肌的保护作用。方法将９６只猫随机分为体外循环（ＣＰＢ）组（Ⅰ）、损伤组（Ⅱ）、冷晶保护组（Ⅲ）及温血保护组（Ⅳ）。观测各组心功能、膜ＡＴＰ酶活性和膜蛋白颗粒的变化。结果组Ⅰ各时间点各项指标无变化。缺血期间,组ⅡⅣＮａＫＡＴＰａｓｅ活性下降（Ｐ＜０．０１）;组Ⅱ、ⅢＣａＭｇＡＴＰａｓｅ活性下降,膜蛋白颗粒数减少（Ｐ＜０．０５）,组Ⅳ无减少（Ｐ＞０．０５）。复灌后,组Ⅳ心功能、ＣａＭｇＡＴＰａｓｅ活性恢复正常,ＮａＫＡＴＰａｓｅ活性和膜蛋白颗粒数恢复稍差。结论单纯ＣＰＢ对心功能、膜蛋白无损伤作用;温血停搏液心肌保护作用较好,但仍需完善。     

单纯钾停跳氧合血持续灌注不降温心脏直视手术(附160例报告)

应用钾停跳、氧合血持续灌注心肌保护、不降温体外循环行心脏直视手术１６０例，手术均顺利，术后无低心排综合征、无严重心律失常发生。全组死亡２例（１．２５％）。部分病例进行了ＬＤＨ１／ＬＤＨ２、ＣＫ－ＭＢ及血清乳酸测定，与低温体外循环组比较无统计学明显差异（Ｐ＞０．０５）。作者认为，此方法临床效果满意，值得进一步研究、推广应用。     

Intermittent Antegrade Tepid Versus Cold Blood Cardioplegia in Elective Myocardial Revascularization

Background. The ideal temperature for blood cardioplegia administration remains controversial.

Methods. Fifty-two patients who required elective myocardial revascularization were prospectively randomized to receive intermittent antegrade tepid (29°C; group T, 25 patients) or cold (4°C; group C, 27 patients) blood cardioplegia.

Results. The two cohorts were similar with respect to all preoperative and intraoperative variables. The mean septal temperature was higher in group T (T, 29.6° ± 1.1°C versus 17.5° ± 3.0°C; p < 0.0001). After reperfusion, group T exhibited significantly greater lactate and acid release despite similar levels of oxygen extraction (p < 0.05). The creatine kinase-MB isoenzyme release was significantly lower in group T (764 ± 89 versus 1,120 ± 141 U · h/L; p < 0.04). Hearts protected with tepid cardioplegia demonstrated significantly increased ejection fraction with volume loading, improvement in left ventricular function at 12 hours, and decreased need for postoperative inotropic support (p < 0.05). The frequency of ventricular defibrillation after cross-clamp removal was lower in this cohort (p < 0.05). There were no hospital deaths, and both groups had similar postoperative courses.

Conclusions. Intermittent antegrade tepid blood cardioplegia is a safe and efficacious method of myocardial protection and demonstrates advantages when compared with cold blood cardioplegia in elective myocardial revascularization.     

Myocardial Distribution of Antegrade Cold Crystalloid and Tepid Blood Cardioplegia

Background. Tepid blood (TB) cardioplegia combines the improved rheologic characteristics and the augmented oxygen and substrate delivery of blood cardioplegia with the advantages of moderate hypothermia. In addition, the intramyocardial distribution of continuous TB cardioplegia may also be better than intermittent cold crystalloid (CC) cardioplegia. We sought to compare the distribution of TB and CC cardioplegia at varying infusion pressures.

Methods. In situ, isolated canine hearts were randomized to antegrade, continuous TB (28°C, n = 8) or intermittent CC (n = 8) cardioplegia infused at 50, 75, and 100 mm Hg. The regional distribution of cardioplegia at each pressure was measured by 15-μm colored microspheres. Cardioplegia distribution was measured from three areas each of the right ventricle (inflow, outflow, and apex) and the left ventricle (anterior, lateral, and posterior). Left ventricular samples were subdivided into subepicardial, midmyocardial, and subendocardial.

Results. Delivery of cardioplegia to all areas of the right and left ventricles showed a linear pressure–flow relationship over the range of pressures tested. Right ventricular distribution was two-thirds of that to the left ventricle, and left ventricular subepicardial distribution was approximately one half of subendocardial flow in both groups at all delivery pressures. However, the subendocardial to subepicardial ratio was significantly greater with TB cardioplegia than with CC cardioplegia. Transmural right ventricular cardioplegia flow was comparable in both groups. In contrast, left ventricular distribution of CC cardioplegia was greater than TB cardioplegia at all three pressures tested.

Conclusions. The pressure–flow relationship in both CC and TB cardioplegia is linear in both the right and left ventricular myocardium over clinically applicable delivery pressures. The distribution of cardioplegia to the right ventricle is not altered by increased pressure.     

逆行性灌注浅低温氧合血心脏不停跳与冷血心脏停搏液对cTn I的影响

目的　对比研究逆行性灌注浅低温氧合血心脏不停跳与低温冷血心脏停搏液对外周血清心肌肌钙蛋白 I(c Tn I)的影响。　方法　将 18例双瓣膜置换术患者分为心脏不停跳组和心脏停搏组 ,观察围手术期外周血清c Tn I、肌酸激酶 (CK)、肌酸激酶同工酶 (CK- MB)及主动脉阻断前后用透射电子显微镜观察心肌超微结构变化。结果　心脏不停跳组主动脉开放后各个时相点 CK虽略低于心脏停搏组 ,但差别无显著性意义 (P>0 .0 5 ) ;主动脉开放后 6小时 CK- MB明显低于心脏停搏组 (P<0 .0 5 ) ,主动脉开放后各个时相点心脏不停跳组 c Tn I明显低于心脏停搏组 (P<0 .0 5 )。两组患者主动脉阻断前心肌超微结构均有轻度改变 ,主动脉阻断 90分钟心脏停搏组心肌超微结构损伤较心脏不停跳组明显。　结论　逆行性灌注浅低温氧合血心脏不停跳围手术期外周血清 c Tn I较低 ,可能与该方法使体外循环期间发生不可逆损伤的心肌细胞较少 ,心肌超微结构损伤较轻有关。     

间断冷血与持续温血灌注心肌保护的对比研究

目的为探索临床上更为安全实用的心肌保护方法，对４０例心脏手术患者用含钾冷氧合血间断灌注与含钾温氧合血持续灌注进行对比研究。方法应用含钾温血持续灌注与含钾冷血间断灌注心肌保护法行心内直视手术各２０例，分别对复跳情况、心肌酶谱（ＡＳＴ，ＣＫ，ＣＫ－ＭＢ，ＬＤＨ）及手术前后心功能变化进行对照分析。结果持续温血组与间断冷血组自动复跳率分别为１８／２０和７／２０（Ｐ＜０．０５），超声心动图测得左心功能参数（手术前ＴＴＥ结果与停机拔管后ＴＥＥ结果之差）：射血分数（ＥＦ）分别为８．６９±６．２％和－１．３０±１２．７３％（Ｐ＜０．０５）；短轴缩短率（ＦＳ）分别为７．６±１０．７％和－１．７３±６．８％（Ｐ＜０．０５）；左心室舒张末内径（ＬＶＥＤＤ）分别为１．３７±０．３１ｃｍ和０．６±０．８８ｃｍ（Ｐ＜０．０５）。两组心肌酶谱无差异（Ｐ＞０．０５）。结论间断冷血灌注心肌保护法在临床上更为安全     

温血停搏液术终灌注对缺血再灌注心肌的保护作用

利用猫体外循环模型观察含甘露醇的温血停搏液术终灌注对缺血再灌注心肌的保护作用。心肌缺血恢复正常血液灌注前，从主动脉根部以５～６ｋＰａ的压力注入３７℃含甘露醇的低钾温血停搏液５０ｍｌ。结果显示用含甘露醇的温血停搏液术终灌注可保护缺血后再灌注心肌的功能，提高心肌能量储备，降低线粒体丙二醛含量。结论：含甘露醇的温血停搏液术终灌注，可提高心肌对氧自由基的清除能力，减轻线粒体膜脂质过氧化，提高心肌能量储备，有利于再灌注后心肌功能的恢复