del Nido心脏停搏液在主动脉夹层手术中的心肌保护效果

摘要 目的：探讨del Nido心脏停搏液在主动脉夹层手术中的心肌保护效果。方法：2015年2月到2020年6月选择在本院进行急诊手术的Stanford A型主动脉夹层的150例患者,入院后根据术中采用的心脏停搏液的不同分为两组 del Nido组与对照组各75例,所有患者都实施大血管外科手术,由同一组医师团队完成手术。Del Nido组给予del Nido心脏停博液灌注,对照组给予改良St. Thomas液灌注,记录心肌保护效果。结果：所有患者完成手术,两组的体外循环时间、停循环时间、阻断主动脉时间对比差异无统计学意义(P>0.05),del Nido组的灌注次数、总灌注时间、停博液晶体总量与对照组对比,差异有统计学意义(P<0.05)。Del Nido组的机械通气时间、ICU停留时间、术后住院时间短于对照组(P<0.05)。两组术后1 d的血清 cTnⅠ高于术前(P<0.05),del Nido组低于对照组(P<0.05)。两组术后7 d的院内死亡、心律失常、开胸止血、肾功能不全、肝功能不全等发生率对比差异无统计学意义(P>0.05)。结论：del Nido心脏停搏液在主动脉夹层手术中的能更好地发挥心肌保护效果,且不增加术后并发症的发生,减少灌注次数、总灌注时间,有利于促进患者康复。     

心肌保护新方法—持续灌注温血心停跳液技术

心肌保护仍是目前需要进一步研究的课题。传统心肌保护研究的焦点集中在如何减轻心脏停搏时的缺血损伤或复灌后的再灌注损伤,研究结果也表明,化学性停搏加局部低温,以及复灌早期的控制性再灌注只能减轻心肌缺血再灌注损伤的程度,并不能完全消除缺血再灌注损伤。因为这些方法没有从根本上解决心脏停搏期间氧的供需矛盾,心肌缺血缺氧不可避免,对于需长时间停搏的心脏和高危病例,传统的心肌保护方法无法提供满意的心肌保护效果。近年来,心肌保护的方法有很大的发展,尤其是新近提出的持续灌注温血心脏停跳液技术,它可使心脏     

含血停搏液镁离子浓度对未成熟心肌保护的影响

目的 采用幼兔离体心脏模型。模拟临床上可能出现的含血停搏液Ca^2 浓度变化,探讨适宜于未成熟心肌保护的Mg^2 浓度。方法 3-4周龄长耳白兔,依照含血停搏液不同Mg^2 浓度（0.6mmol/L,4.0mmol/L,8.0mmol/L,120mmol/L,16.0mmol/L）随机分为5组,建立Langendorff离体心脏灌注模型。采用Ca^2 浓度1.2-1.5mmol/L的含血停搏液,运用温血停搏液诱导停搏,冷血停搏液间断灌注,低温保护,终末温血停搏液控制性再灌注技术,观察以下指标：1、血流动力学指标;实验前后恢复率;心率,主动脉流量,冠脉流量,心排量,左室收缩压和左室舒张末压;2、心肌含水量;3、冠脉流出液乳酸盐含量;4、心肌肌酸激酶和乳酸脱氢酶漏出率;5、心肌细胞内Na^2 ,Ca^2 含量;6、心肌组织ATP含量;7、心肌组织SOD活性,MDA含量;8、心肌超微结构。结果 1、心率恢复率,主动脉流量恢复率及左室收缩压恢复率组间总体差异无显著性。而冠脉流量恢复率,心排量恢复率和左室舒张末压恢复率以Mg^2 浓度8.0mmol/L和12.0mmol/L为优,0.4mmol/L组最差。2、心肌含水量以Mg^2 浓度8.0mmol/L和12.0mmol/L为最低。3、冠脉流出液乳酸盐含量0.4mmol/L组,8.0mmol/L和12.0mmol/L组高于欺科2组。4、心肌乳本能部氢酶漏出率以8.0mmol/L组最低,而肌酸激酶漏出率以8.0mmol/L和12.0mmol/L组为最低。5、心肌细胞内Na^ 、Ca^2 含量;6、心肌组织ATP含量;7、心肌组织SOD活性,MDA含量;8、心肌超微结构。结果：1、心率恢复率,主动脉流量恢复率及左室收缩压恢复率组间总体差异无显著性。而冠脉流量恢复率,心排量恢复率和左室舒张末压恢复率以Mg^2 浓度8.0mmol/L和12.0mmol/L为优,0.4mmol/L组最差。2、心肌含水量以Mg^2 浓度8.0mmol/L和12.0mmol/L为最低。3、冠脉流出液乳酸盐含量0.4mmol/L组最差。2、心肌含水量以Mg^2 浓度8.0mmol/L和12.0mmol/L为最低。3、冠脉流出液乳桎卤含量0.4mmol/L组,8.0mmol/L和12.0mmol/L组高于其余2组。4、心肌乳酸脱氢酶漏出率以8.0mmol/L组最低,而肌酸激酶漏出率以8.0mmol/L和12.0mmol/L组为最低。5、心肌细胞内Na^2 含量以8.0mmol/L和12.0mmol/L组为最低,而心肌细胞内Ca^2 含量以8.0mmol/L组最低。6、心肌组织ATP含量以12.0mmol/L组为最高。7、心肌组织SOD活性以8.0mmol/L和12.0mmol/L组库最高,而MDA含量各组间总体差异无显著性。8、心肌超微结构;8.0mmol/L和12.0mmol/L组表现为基本正常未成熟心肌超微结构,而0.4mmol/L组超微结构有明显损伤表现。结论 对于未成熟心肌,当采用温血停搏液诱导停搏,冷血停搏液间断灌注,低温保护,温血停搏液终末控制性再灌注技术时,为避免含血停搏液Ca^2 浓度偏高对未成熟心肌的不利影响。应维持含血停搏液中Mg^2 浓度在8-12mmol/L。     

心脏晶体停搏液和冷血停搏液不同灌注方法对心肌保护的评价

目的：评估二种心脏停搏液不同灌注方法对心肌保护作用。方法：30例双瓣患者随机分为冷晶体停搏液间断灌注组(n=10),冷血停搏液间断灌注组(n=10),冷血停搏液持续灌注组(n=10),观察血浆心肌肌钙蛋白T(CnT)、肌酸激酶(CK)、肌酸激酶同工酶(CK—MB)。结果：体外循环后冷晶体停搏液间断灌注组血浆心肌肌钙蛋白T和肌酸激酶、肌酶激酶同工酶较其他2组明显增高;冷血停搏液间断灌注组和冷血停搏液持续灌注组血浆心肌肌钙蛋白T、肌酸激酶、肌酸激酶同工酶无明显差异。结论：冷血停搏液的心肌保护优于冷晶体停搏液,冷血停搏液间断灌注与持续灌注没有明显差异。     

左旋精氨酸在冠脉搭桥术中心肌保护效果研究

目的:通过在心脏停搏液中添加适量左旋精氨酸来观察其在冠脉搭桥术中心肌保护效果。方法:选择2008年1月～2010年1月在我院行冠状动脉旁路移植术患者20例,随机分为2组,每组10例,对照组:常规心肌保护液组,不添加左旋精氨酸。实验组,心肌保护液中加入7.5g/L左旋精氨酸。测患者术前(T1)、术后6小时(T2)、术后12小时(T3)、术后24小时(T4)、术后48小时(T5)血浆中TNF-α、IL-6、IL-8及cTn I含量。记录临床观察指标。结果:两组血浆TNF-α、IL-6、IL-8、cTn I浓度术前无统计学意义(P>0.05),术后各时点TNF-α、IL-6、IL-8、cTn I浓度显著升高且实验组均低于对照组(P<0.05)。临床观察指标除血管活性药物应用情况实验组优于对照组(P<0.05)外无明显差异。结论:在心脏停搏液中加入L-精氨酸,可有效保护缺血心肌,减轻心肌再灌注损伤程度。     

左旋精氨酸在冠脉搭桥术中心肌保护效果研究

目的：通过在心脏停搏液中添加适量左旋精氨酸来观察其在冠脉搭桥术中心肌保护效果。方法：选择2008年1月~2010年1月在我院行冠状动脉旁路移植术患者20例,随机分为2组,每组10例,对照组：常规心肌保护液组,不添加左旋精氨酸。实验组,心肌保护液中加入7．5gm左旋精氨酸。测患者术前（T1）、术后6小时（T2）、术后12小时（T3）、术后24小时（T4）、术后48小时（T5）血浆中TNF-α、IL-6、IL-8及cTnI含量。记录临床观察指标。结果：两组血浆TNF-α、IL．6、IL-8、cTnI浓度术前无统计学意义（P〉0．05）,术后各时点TNF-α、1L-6、IL．8、cTnI浓度显著升高且实验组均低于对照组（P〈0．05）。临床观察指标除血管活性药物应用情况实验组优于对照组（P〈0．05）外无明显差异。结论：在心脏停搏液中加入L-精氨酸,可有效保护缺血心肌,减轻心肌再灌注损伤程度。     

177例双瓣替换术的心肌保护和辅助循环的探讨

目的：本文报告了177例双瓣替换术的心肌保护和辅助循环方法。临床9资料：本组病例包括165例主动脉和二尖瓣替换术,8例同时行三尖瓣成形术;4例同时行冠状动脉搭桥术。术前心功能Ⅲ-Ⅳ级,心胸心率54－89％,结果：升主动脉阻断时间48－265分。自动复跳114例,9例作IABP辅助,IAPP时间6－162小时,7例成活,成功率为78％,全组177例住院死亡6例,占死亡3．40％,结论：在体外循环中采用综合的心肌保护和辅助循环的方法的手术成功的关键。     

大鼠心脏低温保存及高钾停跳保护作用的ESR研究

用ESR研究大鼠离体心脏低温长时间缺血后再灌注时产生的自由基,并观察心肌超微结构的变化;对临床心脏直视手术中常用的高钾停跳液的保护作用机理进行了分析。实验结果表明超氧自由基信号强度随缺血温度的降低而明显减弱。高钾停跳液保护的大鼠离体心脏于低温(4℃)缺血后再灌15s,4h内超氧自由基信号强度变化不明显。缺血4h后再灌注,实验组心脏全部于15s内自动复跳,超微结构的变化轻微。以上改变与对照组比较有明显的差异。本实验为低温保存心脏及高钾停跳液的临床应用提供了实验依据。     

1600例重症心脏瓣膜置换术中的体外循环管理

目的报告1600例重症心脏瓣膜置换术中的体外循环管理技术。方法CPB中采用低液面预充、中度血液稀释、浅低温、HCT22～25％,心肌保护为高钾含血停跳液灌注。对心胸比例超过85％,合并肝大、腹水、肺长期淤血的患者,CPB中采用超滤法。结果体外循环时间90～357min,主动脉阻断时间50～170min,心脏停跳时间54～175min,术中灌注压55～70mmHg,中心静脉压0～5cm H2O,尿量平均200～800ml,自动复跳1047例,占65％。结论为了提高重症心脏瓣膜手术的体外循环质量,增加手术成功率,强调：(1)中度血液稀释,提高胶体渗透压;(2)CPB中用高钾含血停搏液作为心肌保护,必须做到按时、足量灌注;(3)及时补充碱性药物和电解质;(4)补充充足的镁离子可增加细胞内的钾离子浓度。     

川芎嗪对缺血心肌的保护及抗氧化作用的实验研究

研究川芎嗪的心肌保护及抗氧化作用机制。在心脏停跳液中加入川芎嗪后对离全兔心脏进行缺血再灌注,然后观察心肌线粒体内丙二醛（ＭＤＡ）含量、超氧化物岐化酶（ＳＯＤ）活性及心肌组织超微结构损伤程度。发现含有川芎嗪的停跳液组丙二醛（ＭＤＡ）含量显著降低,超氧化物岐化酶（ＳＯＤ）活显著升高,观察心肌组织超微结构损伤程度发现较轻,因此,川芎嗪对缺血心肌具有良好的保护脑抗氧化作用。     

Propofol is cardioprotective in a clinically relevant model of normothermic blood cardioplegic arrest and cardiopulmonary bypass

The general anesthetic propofol has been shown to be cardioprotective. However, its benefits when used in cardioplegia during cardiac surgery have not been demonstrated. In this study, we investigated the effects of propofol on metabolic stress, cardiac function, and injury in a clinically relevant model of normothermic cardioplegic arrest and cardiopulmonary bypass. Twenty anesthetized pigs, randomized to propofol treatment (n = 8) and control (n = 12) groups, were surgically prepared for cardiopulmonary bypass (CPB) and cardioplegic arrest. Doses of warm blood cardioplegia were delivered at 15-min intervals during a 60-min aortic cross-clamped period. Propofol was continuously infused for the duration of CPB and was therefore present in blood cardioplegia. Myocardial biopsies were collected before, at the end of cardioplegic arrest, and 20 mins after the release of the aortic cross-clamp. Hemodynamic parameters were monitored and blood samples collected for cardiac troponin I measurements. Propofol infusion during CPB and before ischemia did not alter cardiac function or myocardial metabolism. Propofol treatment attenuated the changes in myocardial tissue levels of adenine nucleotides, lactate, and amino acids during ischemia and reduced cardiac troponin I release on reperfusion. Propofol treatment reduced measurable hemodynamic dysfunction after cardioplegic arrest when compared to untreated controls. In conclusion, propofol protects the heart from ischemia-reperfusion injury in a clinically relevant experimental model. Propofol may therefore be a useful adjunct to cardioplegic solutions as well as being an appropriate anesthetic for cardiac surgery.     

Myocardial interstitial glucose and lactate before,during, and after cardioplegic heart arrest

The interstitial fluid of the human myocardium was monitored in 13 patients undergoing aortic valve and/or bypass surgery before, during, and after hypothermic potassium cardioplegia. The regulation of glucose and lactate was studied after sampling with microdialysis. The following questions were addressed. 1). Is the rate of transcapillary diffusion the limiting step for myocardial uptake of glucose before or after cardioplegia? 2). Does cold potassium cardioplegia induce a critical deprivation of glucose and/or accumulation of lactate in the myocardium? Before cardioplegia, interstitial glucose was approximately 50% of the plasma level (P < 0.001). Interstitial glucose decreased significantly immediately after induction of cardioplegia and remained low (1.25 +/- 0.25 mM) throughout cardioplegia. It was restored to precardioplegic levels 1 h after release of the aortic clamp. Interstitial glucose then decreased again at 25 and 35 h postoperatively to the levels observed during cardioplegia. Interstitial lactate decreased immediately after induction of cardioplegia but returned to basal level during the clamping period. At 25 and 35 h, interstitial lactate was significantly lower than before and during cardioplegia. Glucose transport over the capillary endothelium is considered rate limiting for its uptake in the working heart but not during cold potassium cardioplegia despite the glucose deprivation following perfusion of glucose-free cardioplegic solution. Lactate accumulated during cardioplegia but never reached exceedingly high interstitial levels. We conclude that microdialysis provides information that may be relevant for myocardial protection during open-heart surgery.     

Electrical activity of the heart in anti-ischemic protection of the myocardium

The paper studies electrical activity of the heart during the anti-ischemic protection by cool high-potassium cardioplegic solution based on the blood. Parametres characterising automatism function and the myocardial state of the ventricles practically did not differ from the control data obtained during the experiments without ischemia. Atrioventricular conduction and the atrium myocardium were worse preserved. The positive effects of the papaverine addition to the cardioplegic perfusate has been also shown. The author came to the conclusion that it is necessary to pay special attention to the electrical activity of the supraventricular area of the heart for the adequate evaluation of the cardioplegia.     

Warm blood cardioplegia reduces the fall in the intracellular concentration of taurine in the ischaemic/reperfused heart of patients undergoing aortic valve surgery

Summary The effect of cold and warm intermittent antegrade blood cardioplegia, on the intracellular concentration of taurine in the ischaemic/ reperfused heart of patients undergoing aortic valve surgery, was investigated. Intracellular taurine was measured in ventricular biopsies taken before institution of cardiopulmonary bypass, at the end of 30 min of ischaemic arrest and 20 min after reperfusion. There was no significant change in the intracellular concentration of taurine in ventricular biopsies taken after the period of myocardial ischaemia in the two groups of patients (from 10.1 ± 1.0 to 9.6 ±0.9mol/g wet weight for cold and from 9.3 ± 1.3 to 10.0 ± 1.3mol/g wet weight for warm cardioplegia, respectively). Upon reperfusion however, there was a fall in taurine in both groups but was only significant (P 0.05) in the group receiving cold blood cardioplegia (6.9 ± 0.8mol/g wet weight after cold blood cardioplegia versus 8.0± 0.8mol/g wet weight following warm blood cardioplegia). Like taurine, there were no significant changes in the intracellular concentration of ATP after ischaemia in the two groups of patients (from 3.2 ± 0.32 to 2.95 ± 0.43mol/g wet weight for cold and from 2.75 ± 0.17 to 2.62 ± 0.21mol/g wet weight for warm cardioplegia, respectively). However upon reperfusion there was a significant fall in ATP in both groups with the extent of the fall being less in the group receiving warm cardioplegia (1.79 ± 0.19mol/g wet weight for cold and 1.98 ± 0.27mol/g wet weight for warm cardioplegia, respectively). This work shows that reperfusion following ischaemic arrest with warm cardioplegia reduces the fall in tissue taurine seen after arrest with cold cardioplegia. Accumulation of intracellular sodium provoked by hypothermia and a fall in ATP, may be responsible for the fall in taurine by way of activating the sodium/taurine symport to efflux taurine.     

Intraoperative myocardial protection by potassium arrest and local cardiac hypothermia

The combined modalities of potassium arrest and local cardiac hypothermia were used for myocardial protection in 82 patients. The cardioplegic solution used was Ringer's lactate to which potassium chloride and sodium bicarbonate were added so that the final solution had a pH of 7.5 and 30 meq/liter potassium. The myocardium was cooled externally by cold Ringer's lactate at 4 °C and through coronary circulation by cold cardioplegic solution at 8 °C. The myocardial temperature was continuously monitored and kept between 12 and 18 °C. Moderate systemic hypothermia was used (26 to 30 °C). Eighty-two patients have been operated upon using this technique. Eighteen patients had single or double valve replacements, 4 had valve replacements with coronary bypass, and 60 had coronary bypass procedures. The operating conditions have been excellent and the myocardial protection offered by this technique has been good. Perioperative myocardial infarctions, as diagnosed by ECG and CPK (MB isoenzymes) and myocardial scans, were seen in 6 patients. In conclusion the combined modalities of potassium arrest and local cardiac hypothermia give excellent myocardial protection during cardiac surgery.     

Effect of cardioplegia on nitrogen and energy metabolism of the human heart

The interrelation between the energy and nitrogenous metabolism of the myocardium during cardioplegia has been studied in patients with congenital valvular heart disease (tetralogy of Fallot--12 patients, ventricular septal defect--5 patients). Whole body hypothermia with repeated heart reperfusion with cold cardioplegic blood perfusate was used for the protection of the myocardium. However, ATP level of the myocardium of some patients decreased by 20% and more of the baseline. This loss was accompanied by a reduction in glutamate and aspartate levels and a rise in ammonium and alanine levels in the myocardium (by 17.7 +/- 3.8; 17.6 +/- 5.9; 61.4 +/- 12.5 and 92.4 +/- 26.3% of the baseline, respectively).