开放主动脉前灌注含甘露醇的温血停搏液对心肌MDA和SOD…

利用猫体外循环模型。观察心有缺血再灌注过程中ＭＤＡ，ＳＯＤ的变化，开放主动脉再灌注含甘露醇的温血停搏液对其影响。结果见缺血心肌再灌注后线粒体ＭＤＡ含量明显增，缺血心肌复灌前从主动脉根部注入含甘露醇温血停搏液，使心脏在有氧下停搏，可降低心肌线粒体ＭＤＡ含量，提高心肌ＳＯＤ活性，表明缺血心肌在恢复正常血供前灌注含甘露醇温血停搏液，可减轻膜脂质的过氧化，保护自由基清除系统，减轻心肌的再灌注损伤。     

开放主动脉前灌注含甘露醇的温血停搏液对心肌MDA和SOD的影响

利用猫体外循环模型，观察心肌缺血再灌注过程中ＭＤＡ、ＳＯＤ的变化，及开放主动脉前灌注含甘露醇的温血停搏液对其影响。结果见缺血心肌再灌注后线粒体ＭＤＡ含量明显增加；缺血心肌复灌前从主动脉根部注入含甘露醇温血停搏液，使心脏在有氧环境下停搏，可降低心肌线粒体ＭＤＡ含量，提高心肌ＳＯＤ活性。表明缺血心肌在恢复正常血供前灌注含甘露醇温血停搏液，可减轻膜脂质的过氧化，保护自由基清除系统，减轻心肌的再灌注损伤。     

温血停搏液术终灌注对缺血再灌注心肌线粒体功能的影响

利用猫体外循环模型观察心肌缺血后温血停搏液再灌注对线粒体功能的影响。结果发现，心肌缺血６Ｏｍｉｎ时，线粒体功能呈现下降趋势，但与正常组相比，相差不显著。单纯再灌注组恢复正常血供６０ｍｉｎ后，线粒体功能进一步下降，同正常组或缺血组相比，相差非常显著。而温血停搏液再灌注可保护线粒体功能，同单纯再灌注组相比，两者相差显著表明心肌急性缺血后温血停搏液再灌注可减轻心肌线粒体再灌注损伤。     

温血停搏液诱导及末次灌注心肌的保护作用

将温血停搏液诱导及末次灌注应用于临床２０例成人人工瓣膜替换术术中心肌保护。２０例均恢复顺利，无１例术后早期死亡。诱导心脏停搏较快，均于温血停搏液２分钟诱导完毕前停搏。自动复跳率及房颤转窦率均高。术中心肌三磷酸腺苷测定发现此法能保存更多的心肌能量物质。术中及术后血清中肌酸磷酸激酶测定见其术后升高低于对照组，且恢复也较快，提示心肌细胞损伤较轻。本法易于施行。实验及临床均证实其对术中缺血心肌保护的效果优于传统的冷钾晶体停搏液，有推广前景。     

氨基酸盐温血停搏液诱导和末次灌注对缺血犬心肌的保护作用

为研究氨基酸盐温血停搏液诱导和末次灌注对缺血犬心肌的保护作用,应用犬体外循环工作模型,心肌缺血120分钟。动物随机分为3组,Ⅰ组:温血停搏液诱导和末次灌注,中间用st.Thomas’NO.2液(STS)冷晶体停搏液;Ⅱ组同Ⅰ组,但诱导与末次灌注温血停搏液中含L—门冬氨酸(L-asperte,A)和L—谷氨酸钠(L-glutamate,G)各13mmol/L;Ⅲ组同Ⅱ组,但STS液中亦含相同浓度的氨基酸(AG)。结果表明,缺血复灌后,AG用于温血和冷晶体停搏液中(Ⅱ、Ⅲ组),心功能恢复明显改善,Ⅲ组在缺血后心肌ATP含量明显高于Ⅰ组(P<0.05)。心肌超微结构Ⅲ组缺血前后无明显改变。本实验提示:温血及冷停搏液中含AG进一步加强了心肌保护作用。     

温血心脏停搏液持续灌注对长时间停搏心肌的保护作用

目的利用猫体外循环模型对比观察间断冷血、持续冷血及持续温血心脏停搏液灌注对长时间停搏心肌的保护作用。方法健康猫２４只，随机分成４组：Ⅰ组为正常对照组，取正常猫心测定有关指标做为正常对照；Ⅱ～Ⅳ组为心脏停搏组，停搏时间３小时，用不同心肌保护方法保护心肌。结果心脏停搏３小时后心肌线粒体呼吸功能、氧化磷酸化能力及心肌三磷酸腺苷（ＡＴＰ）含量在间断冷血组明显下降，持续冷血组呈轻度下降，持续温血组保持正常。结论持续灌注温血停搏液技术可使心脏在停搏期间有充足的血液供应，是一种理想的心肌保护方法，特别适用于需长时间停搏和高危病例。     

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。     

冷晶体间断灌注与联合温血诱导停搏及终末再灌注的对比研究

目的　对比温氧合血诱导停搏及终末再灌注和 4℃冷晶体心脏停搏液间断灌注的心肌保护作用。　方法将 4 0例风湿性心脏病患者随机等分成温血组和冷晶体组 ,观察心脏自动复跳率 ,测定停搏前、复跳后 0小时、6小时、12小时、18小时、2 4小时和 4 8小时的血浆心肌肌钙蛋白 I(c Tn I) ,对心肌线粒体作量化计分。　结果　温血组心脏自动复跳率明显高于冷晶体组 ;体外循环后温血组 c Tn I明显低于冷晶体组 ,温血组 c Tn I高峰出现时间较早 ;线粒体量化计分分数反映复跳后温血组心肌损伤较轻。　结论　温氧合血诱导停搏及终末再灌注的心肌保护效果较好。     

温血停搏液诱导和（或）末次灌注心肌保护的应用

温血停搏液诱导和（或）末次灌注心肌保护的应用蓝鸿钧，孙宗全，杜心灵，徐志娟，冯汉屏１９９２年１月至１９９３年１月我们用温血停搏液诱导和（或）末次灌注于２６例人工瓣膜替换术病人的心肌保护，取得良好效果。现报道如下：方法温血停搏液采用转流后混匀的机器血，...     

温血心脏停搏液持续灌注对长时间停博心肌的保护作用

目的 利用猫体外循环模型对比观察间断冷血、持续冷血及持续温血心脏停搏液灌注对长时间停搏心肌保护的作用。方法 健康猫２４只，随机分成４组：Ⅰ组为正常对照组，取正常猫心测定有关指标做为正常对照；Ⅱ－Ⅳ组为心脏停搏组，停搏时间３小时，用不同心肌保护方法保护心肌。结果 心脏停搏３小时后心肌线粒体呼吸功能、氧化磷酸化能力及心肌三磷酸腺苷（ＡＴＰ０含量在间断冷血组明显下降，持续冷血组呈轻度下降，持温血组保持正     

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     

Experimental evaluation of myocardial protective effect of prostacyclin analog (OP-41483) as an adjunct to cardioplegic solution

A stable prostacyclin analog (OP-41483) was evaluated for myocardial protective effect against global ischemia with the use of cardioplegia. Isolated canine hearts (n = 25) were exposed to 60 minutes of warm (37 degrees C) global ischemia after the arrest by crystalloid cardioplegia. Prostaglandin analog was given in three different ways: preadministration (700 ng/kg body weight per minute) before ischemia for 30 minutes (group I, n = 5), given as a component of cardioplegic solution (600 ng/ml, group II, n, = 6), and post-administration (25 ng/kg body weight per minute) during reperfusion for 30 minutes (group III, n = 7). During reperfusion, coronary sinus blood flow, 6-keto-prostaglandin F1 alpha in coronary sinus blood, and myocardial oxygen consumption were measured during reperfusion. As a result, groups II and III showed significantly better global left ventricular function (developed pressure, maximum dP/dt, and diastolic compliance) than the control group (without prostaglandin analog, n = 7) and group I. Myocardial oxygen consumption at reperfusion (1 minute) was significantly larger in group II than in the control group. 6-keto-prostaglandin F1 alpha flux was significantly larger in group II than in the other three groups during reperfusion. The results indicated that prostaglandin analog has a beneficial effect on myocardial protection under global ischemia with cardioplegia, particularly when used as a component of cardioplegic solution and also during reperfusion. The mechanism may relate to the cytoprotective effect (including protection of endothelium with enhanced endogenous prostacyclin production at reperfusion and also to the modulation of reperfusion per se.     

Effects of supplemental L-arginine during warm blood cardioplegia.

OBJECTIVES: Effects of supplemental L-arginine, nitric oxide precursor, during warm blood cardioplegia were assessed in the blood perfused isolated rat heart. METHODS: The isolated hearts were perfused with blood at 37 degrees C from a support rat. After 20 minutes of aerobic perfusion, the hearts were arrested for 60 minutes with warm blood cardioplegia given at 20-minute intervals. This was followed by 60 minutes of reperfusion. The hearts were divided into the following three groups according to the supplemental drugs added to the cardioplegic solution. The control group (n = 10) received standard warm blood cardioplegia. The L-ARG group (n = 10) received warm blood cardioplegia supplemented with L-arginine (3 mmol/l). The L-NAME group (n = 10) received warm blood cardioplegia supplemented with L-arginine (3 mmol/l) and L-nitro-arginine methyl ester, a competitive inhibitor of nitric oxide synthase (1 mmol/l). After 60 minutes of cardioplegic arrest, cardiac function, myocardial metabolism and myocardial release of circulating adhesion molecules were measured during reperfusion. RESULTS: Left ventricular end-diastolic pressure was significantly lower (p<0.05) in the L-ARG group than in the control group and the L-NAME group during reperfusion. Isovolumic left ventricular developed pressure, dp/dt and coronary blood flow were significantly greater (p< 0.05) in the L-ARG group during reperfusion. The L-ARG group resulted in early recovery of lactate metabolism during reperfusion. Myocardial release of circulating intercellular adhesion molecule-1 (ICAM-1) and E-selectin were significantly less (p<0.05) in the L-ARG group at 15 minutes of reperfusion. CONCLUSIONS: The results suggest that augmented nitric oxide by adding L-arginine to warm blood cardioplegia can preserve left ventricular function and ameliorate endothelial inflammation. The technique can be a novel cardioprotective strategy in patients undergoing cardiac surgery.     

Effects of Hot shot on recovery after hypothermic ischemia in neonatal lamb heart

BACKGROUND: Terminal warm blood cardioplegia, "Hot shot", is the method for providing an energy replenishment and/or early recovery of aerobic metabolism without electromechanical activity at initial reperfusion. The mechanism of beneficial effects of this Hot Shot is multifactorial. This study was designed to assess the effects of terminal warm blood cardioplegia by comparing with oxygenated terminal warm crystalloid cardioplegia. METHODS: In Group HS-B, n=8 (oxygenated blood; 37 degrees C, Ht: 20%, K+ 20 mEq/l, pH 7.237, PO2 219 mmHg) and in Group HS-C, n=8 (bloodless oxygenated (5% CO2+95%O2) crystalloid, 37 degrees C, K+ 20 mEq/l, pH 7.435, PO2 624 mmHg), terminal warm cardioplegia (20 ml/kg for 5 minutes) was studied in the isolated blood perfused neonatal lamb heart following 2 hr of cardioplegic ischemia. Another eight hearts served as control without any kind of terminal cardioplegia. After 60 min of reperfusion, LV function was measured. Coronary blood flow (CBF), oxygen content, and oxygen consumption (MVO2) were measured and the oxygen extraction ratio was calculated in Group HS-B and HS-C during terminal cardioplegia and/or reperfusion. Results are given as % recovery of preischemic values. RESULTS: HS-B as well as HS-C groups showed better functional recovery in maximum developed pressure (DP: 78.0+/-8.3 in HS-B vs 65.2+/-9.2%; p=0.018), maximum dp/dt (67.3+/-6.2 in HS-B, 65.3+/-7.4 in HS-C vs 55.8+/-5.0%; p=0.003, p=0.02), DP V10 (87.1+/-8.5 in HS-B vs 67.2+/-9.9%; p=0.0001), and peak dp/dt V10 (76.4+/-7.6 in HS-B, 69.8+/-8.1 in HS-C vs 58.6+/-6.9 %; p=0.0001) than the control group. Between the HS-B and HS-C groups, HS-B showed better functional recovery in terms of DP V10 (p=0.01). Oxygen delivery of terminal cardioplegia was almost four times higher in HS-B group (90.4+/-17.7 vs 18.7+/-1.1 mcl/ml), contrarily, HS-C group showed four times higher oxygen extraction ratio compared to HS-B group (0.78+/-0.06 vs 0.18+/-0.11), thus oxygen consumption during hot shot was maintained at the same level in both groups. CBF in the control group was lower than that in the other groups at 60 min of reperfusion. CONCLUSIONS: Reperfusion with both terminal warm cardioplegia including blood and oxygenated crystalloid cardioplegia resulted in better recovery of function and higher levels of CBF with slightly better function in terminal warm blood cardioplegia.     

Intermittent warm blood cardioplegia —An experimental study—

The influence of intermittent warm blood cardioplegia (WBCP) on myocardial function and metabolism was studied. Fourty-two adult mongrel dogs were used. The isolated heart of one dog was perfused by the cross circulation method with another support dog. The dogs then were divided into three groups. In group I (n=6), the empty beating heart was perfused with warm blood (WB) kept at 36°C for 100 minutes. In group II (n = 7), the arrested heart was perfused with continuous WBCP using modified Fremes solution for 100 minutes. In group III (n=8), the arrested heart was perfused with WBCP for 10 minutes following a 15-minute non-perfusion period. This perfusion method was repeated four times. The E max, LV developed pressure, ± LV dp/dt and LVEDP were all measured to evaluated the myocardial function. In addition, the coronary venous blood pH, myocardial oxygen consumption, myocardial lactate extraction, coronary blood flow, myocardial high energy phosphate content and myocardial water content were also studied in order to elucidate the myocardial metabolism. Regarding the myocardial function, no significant difference was observed between the three groups. The results of chemical studies on the myocardial metabolism were as follows: (1) the coronary venous blood pH in group III decreased at the end of the no perfusion period of WBCP. But it thereafter gradually returned to the normal physiological range; (2) the myocardial oxygen consumption in group III increased just after each interruption, but then gradually decreased toward following intermittent WBCP; (3) the myocardial lactate extraction decreased at the end of the non-perfusion period. However, it gradually returned to the control value by the end of each period of WBCP perfusion; (4) after 60 minutes of reperfusion, the coronary venous blood pH, myocardial oxygen consumption and myocardial lactate extraction showed no significant differences between the groups; (5) the coronary blood flow in group III increased significantly after 1 minute of reperfusion; (6) the ATP value in group III decreased significantly after 60 minutes of reperfusion. The ADP and AMP values demonstrated no significant difference between the groups during the same period; and (7) no significant difference was seen in the myocardial water content between the groups after 60 minutes of reperfusion. It is thus concluded that 10 minutes of intermittent WBCP followed by a 15-minute interruption appeared to have no deleterious effect on the myocardial funciton and metabolism.     

Effects of angiotensin-converting enzyme inhibitor during warm blood cardioplegia

BACKGROUND: Effects of captopril, an angiotensin-converting enzyme inhibitor, during warm blood cardioplegia were assessed in the blood-perfused, isolated rat heart. METHODS: The isolated hearts were arrested for 60 minutes with warm blood cardioplegia given at 20-minute intervals and were reperfused for 60 minutes. The control group (n = 10) received standard cardioplegia and the captopril group (n = 10) received cardioplegia supplemented with captopril (2 mmol/L). Cardiac function, myocardial metabolism, and cardiac release of circulating adhesion molecules were assessed before and after cardioplegic arrest. RESULTS: Left ventricular end-diastolic pressure and -dp/dt were significantly (p<0.05) lower and coronary blood flow was significantly (p<0.05) greater in the captopril group than the control group during reperfusion. The captopril group resulted in significantly (p<0.05) less cardiac release of lactate, thiobarbituric acid reactive substances during reperfusion. Cardiac release of intercellular adhesion molecule-1 was significantly (p<0.05) less in the captopril group at 60 minutes of reperfusion. CONCLUSIONS: The results suggest that supplementation of captopril during warm blood cardioplegia provides superior myocardial protection by suppressing lipid peroxidation and leukocyte-endothelial cell interaction during reperfusion.     

利多氟嗪加强间断缺血心停搏心肌保护作用的实验研究

报道常温下用利多氟嗪（ｌｉｄｏｆｌａｚｉｎｅ）预处理加强间断主动脉阻断心停搏心肌保护作用的实验研究。１６只犬随机分为对照组和实验组。结果发现，实验组心脏血流动力学的恢复要明显优于对照组。二组间心肌组织ＡＴＰ、腺苷和肌苷以及冠脉回流液中ＣＰＫ、ＣＰＫＭＢ、ＬＤＨ、ＳＯＤ和ＭＤＡ值均有显著性差异（Ｐ＜０．０１）。结论：冠脉搭桥术中采用间断缺血心停搏时加用利多氟嗪有利于保存心肌能量，减轻心肌再灌注损伤和术后迅即恢复心脏功能     

Orthotopic transplantation of pig hearts harvested after 30 min of normothermic ischemia: controlled reperfusion with blood cardioplegia containing the Na-H-exchange inhibitor HOE 642

Objectives: The aim of our study was to develop a surgical technique for a successful transplantation of hearts harvested after 30 min of normothermic ischemia without donor pretreatment. Successful transplantation of ischemic compromised hearts could help to expand the severely limited donor pool. We used the pig model because this species is very susceptible to myocardial ischemia. Na⁺-H⁺-exchange (NHE) inhibitors have shown excellent protective properties in several in vitro and in vivo models of myocardial ischemia and reperfusion. Methods: In group I (n=12) hearts were harvested after 30 min of normothermic ischemia following cardiac arrest induced by exsanguination. Hearts were perfused with warm blood cardioplegia and transplanted orthotopically. In group II (n=9) controlled reperfusion with cold leucocyte-depleted blood cardioplegia was performed after 30 min of normothermic ischemia. In group III (n=8) the same procedure was performed as in group II but blood cardioplegia contained 1 mmol/l HOE 642. Results: In group I massive myocardial oedema was observed and none of the animals could be weaned from cardiopulmonary bypass (CPB). In contrast, all animals in groups II and III could be weaned from CPB with low dose inotropic support. In groups II and III the contractility of the hearts, expressed as maximal left and right ventricular stroke work index was significantly impaired after transplantation as compared with the preoperative value. Supplementation of blood cardioplegia with HOE 642 resulted in a significantly better recovery of the LVSWImax (Group II vs. III). Conclusions: Successful transplantation of pig hearts is possible after 30 min of normothermic ischemia without donor pretreatment if a controlled reperfusion with cold leucocyte-depleted blood cardioplegia is performed. HOE 642 given during reperfusion only improves posttransplant left ventricular function.     

迷走神经预调对心肌缺血再灌注损伤预防作用的实验研究

目的：探讨心脏迷走神经预调对心脏缺血再灌注损伤的预防作用及其机制,以建立一种新的围手术期心肌保护方法。方法：实验用健康杂种犬１６只,随机均分为对照且（Ｃ组）和迷走神经预调组（Ｐ组）。常规建立体外循环,分别于主动脉阻断前以３０Ｈｚ,０．５ｍｓ,１０Ｖ方波刺激心脏迷走神经３ｍｉｎ,间隔３ｍｉｎ,重复２次。转流前、主动脉阻断前、复跳即刻,再灌注３０ｍｉｎ,６０ｍｉｎ时测心输出量（ＣＯ）,射血分数（ＥＦ）     

红细胞停搏液的心肌保护作用及对细胞间粘附分子-1表达的影响

目的：研究红细胞停搏液的心肌保护作用及其对细胞间粘附分子－1表达的影响。方法：应用滤器去除血液中的白细胞和血小板，配制红细胞停搏液，并应用Langendorff离体心模型，测定心率（HR）、左室收缩压峰值（LVSP）、左室舒张末压（LVEDP）、左室内压最大小升速率（dp/dtmax）、冠脉流量（CF）、肌酸激酶（CK）、电镜下观察组织结构的变化，用免疫组化方法观察粘附分子（ICAM－1）的表达情况。结果：在HR、LVSP、dp/dtmax、CF的恢复率、组织显微结构和ICAM－1表达方法，红细胞停搏液组优于全血及去白细胞停搏液组（P＜0．05）。结论：红细胞停搏液较全血停搏液和去白细胞停搏液具有更好的心肌保护作用。