Na+通道阻滞极化停搏液在离体大鼠心脏保存中的保护作用

目的 研究含Na⁺通道阻滞剂河豚毒素(TTX)极化停搏液在离体大鼠心脏保存中的心肌保护作用。方法 20只Wistar大鼠随机均分入St.Thomas去极化停搏组(对照组,Ⅰ组)和TTX极化停搏组(Ⅱ组)。建立离体心脏灌注模型,灌注10min后,分别用St.Thomas和TTX极化停搏液2ml经主动脉插管注入,使心脏停搏。随后将鼠心置于相应配伍的停搏液中,10℃保存7h后重新灌注心脏30min。观察两组心脏保存前后在左心室收缩末压力和压力变化速率恢复率、心肌酶漏出、ATP含量和心肌超微结构等方面的改变。结果 再灌注后,TTX极化停搏组血流动力学各项指标恢复率明显高于Ⅰ组(P<0.01),肌酸磷酸激酶和乳酸脱氢酶漏出量低于Ⅰ组(P<0.05),ATP含量维持在较高水平(P<0.01),心肌超微结构得到较好保护。结论 在离体大鼠心脏低温保存过程中TTX极化停搏液心肌保护作用优于STH液。     

线粒体ATP敏感性钾通道开放剂改善大鼠心脏冷保存

目的:探讨线粒体ATP敏感性钾通道开放剂二氮嗪 (DE)对离体大鼠心脏冷保存效果的影响及作用机制.方法:SD大鼠随机分成对照组、DE组、DE 5-HD组.利用Langendorff离体鼠心灌注法,各组心脏在4℃条件下分别保存3 h和8 h后,复灌60 min,观察各组大鼠血流动力学的恢复情况、冠脉流出液中心肌酶漏出量、心肌水含量的变化及心肌超微结构改变.结果:在Celsior心麻痹液中添加30 μmol/L的DE后,能明显改善冷保存3 h心脏的左心室发展压力的恢复,降低心肌酶(LDH、CK)在某些复灌时间点上的漏出,但对保存后左心室舒张末期压力的抬高和冠脉流量的恢复及心肌水肿程度无明显作用;而相同浓度的DE添加到Celsior心麻痹液中,可明显降低冷保存8 h心脏左心室舒张末期压力的抬高,改善左心室发展压力和冠脉流量的恢复,降低心肌酶(LDH、CK、GOT)的漏出,缓解心肌水肿,对心肌的超微结构也有较好的保护作用,其中30和45 μmol/L DE组对冷保存8 h心脏的保护作用优于15 μmol/L DE组,而3 0及45 μmol/L DE组之间并无显著性差异.DE的上述作用可被线粒体ATP敏感性钾通道的特异性阻断剂5-HD所取消.结论:DE可通过激活线粒体ATP敏感性钾通道显著改善离体大鼠心脏冷保存效果.     

极化心脏停搏液对成熟心肌细胞保护作用的研究

目的观察Na＋通道阻滞剂河豚毒素（TTX）极化心脏停搏液对离体成熟大鼠心肌细胞[Na＋]i、[Ca2＋]i的影响,探讨其对成熟心肌细胞的保护作用。方法成年Wistar大鼠心脏,用酶解法分离成具有搏动性的单个成熟心室肌细胞悬液,随机分成基础组、STH2组（对照组）和TTX组（实验组）,STH2组和TTX组分别应用St.Thomas II号停搏液和TTX停搏液处理,建立模拟缺血/再灌注损伤的停搏/复搏细胞模型,激光扫描共聚焦显微镜（LSCM）测定各组细胞不同时期的[Na＋]i和[Ca2＋]i。结果 TTX组和STH2组成熟心肌细胞复搏后[Na＋]i、[Ca2＋]i均明显高于基础组（P〈0.01）,但TTX组明显低于STH2组（P〈0.01）。结论极化心脏停搏液较去极化心脏停搏液能减轻成熟心肌细胞Na＋、Ca2＋超载,对成熟心肌细胞有较好的保护作用。     

TTX通过JAK2/STAT3通路活化SOD减轻心肌细胞凋亡

目的:研究JAK2/STAT3信号通路在河豚毒素(Tetrodotoxin,TTX)心脏停搏液心肌保护中的作用.方法:24只Wistar大鼠随机均分为对照组、TTX组和TTX+AG490组,每组8只.对照组:开胸取左心室肌作为缺血前对照.TTX组:建立离体心脏Langendorff-Neely灌注模型,预灌注K-H缓冲液30rain后,灌注4℃ TTX心脏停搏液,停搏心脏并低温维持60 min,复灌K-H缓冲液60 min后,取左心室肌备用.TTX+AG490组:操作同℃组,但预灌和复灌时均在K-H缓冲液中加入JAK2抑制剂AG490(5μmol/L).分别采用免疫组化法、比色法和TUNEL法测定心肌组织中p-STAT3、SOD活性和MDA含量.以及心肌细胞凋亡指数(Apoptosis index,AI),并比较组间的变化.结果:与对照组相比,TTX组和TTX+AG490组p-STAT3表达量均明显增加(P<0.05);予以AG490处理后,p-STAT3表达量较TTX组明显下降(p<0.05 )与对照组相比,TTX组和TTX+AG490组SOD活性和MDA含量均明显增加(P<0.05);予以AG490处理后,SOD活性较TTX组显著降低(P<0.05),MDA含量却明显增加(P<0.05 ).经历缺血再灌注后,TTX组和TTX+AG490组心肌细胞AI明显高于对照组(P<0.05);与TTX组相比,TTX+AG490组AI显著增加(P<0.05).结论:JAK2/STAT3信号通路通过增强SOD活性,减轻膜脂质过氧化损伤,减少心肌细胞凋亡,介导TTX心脏停搏液对缺血心肌的保护作用.     

附加N-乙酰半胱氨酸心麻痹液对低温缺血再灌注大鼠心脏高能磷酸化合物代谢的保护作用

目的 应用^31P-核磁共振(^31P-NMR)技术探讨附加N-乙酰半胱氨酸(NAC)心麻痹液对离体低温缺血再灌注鼠心高能磷酸化合物代谢的保护作用。方法 建立^31P-NMR条件下的Langendorff离体心脏逆灌模型，动态测定离体大鼠心脏低温缺血90min再灌注30min过程中的心肌高能磷酸化合物代谢状况，评价附加NAC心麻痹液的作用。结果 附加NAC心麻痹液灌注明显改善再灌注中心肌PCr、ATP和Pi的恢复，显著优于St.Thomas液灌注者。结论 附加NAC可显著改善低温缺血再灌注心脏高能磷酸化合物代谢的保护作用。     

乌拉坦增强延长离体大鼠心脏的低温保存效果

目的：观察乌拉坦对延长离体大鼠心脏的低温保存作用.方法：成年雄性SD大鼠分为两组（n=6）：对照组：HTK保存液; 试验组：HTK保存液加乌拉坦（30mmol/L）.心脏分别置入两种保存液4℃下保存6和18h.采用Langendorff心脏灌注装置进行保存前及保存后再灌注30min时心脏功能测定,比较心脏功能恢复率、ATP含量、细胞凋亡和超微结构变化.结果：低温保存后实验组左室功能恢复率较对照组明显升高,细胞凋亡及超微结构损伤较对照组减轻; 保存18h后实验组ATP含量显著高于对照组.结论：乌拉坦加入HTK心脏保存液能够显著增强离体大鼠心脏的低温保存效果.     

低温含血保护液微流量持续灌注对热缺血猪心的保护

目的研究低温含血保护液微流量持续灌注对热缺血猪心的保护作用,探讨心脏移植中供心保护的有效方法。方法24只离体猪心随机分为实验组（n=12,热缺血10min,4℃含血保护液持续灌注8h）和对照组（n=12,热缺血10min,4℃保护液浸泡保存8h）,进行原位心脏移植,分别监测心脏复跳及血流动力学情况：心率（HR）、平均动脉压（MAP）、心输出量（CO）,心肌肌钙蛋白T（cTnT）、肌红蛋白（Mb）水平。结果实验组心脏复跳情况、血流动力学优于对照组;对照组心肌蛋白显著高于实验组（P〈0．05）。结论低温含血保护液微流量持续灌注对热缺血猪心的心功能以及心肌组织有较好的保护作用。     

JAK2/STAT3通过上调HSP70蛋白介导TTX心肌保护作用

目的研究JAK2/STAT3信号通路在河豚毒素（tetrodotoxin,TTX）心脏停搏液心肌保护中的作用。方法 24只Wistar大鼠随机均分为对照组、TTX组和TTX＋AG 490组,每组8只。对照组：开胸取左心室肌作为缺血前对照。TTX组：建立离体心脏Langendorff-Neely灌注模型,预灌注K-H缓冲液30min后,灌注4℃TTX心脏停搏液,停搏心脏并低温维持60min,复灌K-H缓冲液60min后,取左心室肌备用。TTX＋AG490组：操作同TTX组,但预灌和复灌时均在K-H缓冲液中加入JAK2抑制剂AG490（5μmol/L）。采用免疫组化法测定心肌组织中p-STAT3（磷酸化STAT3）和HSP 70表达量（protein expression index,PEI）,TUNEL检测心肌细胞凋亡指数（apoptosis index,AI）,比较组间的变化。结果与对照组相比,TTX组和TTX＋AG490组心肌组织中p-STAT3和HSP 70的表达量均明显增加（P〈0.05）;予以AG490处理后,p-STAT3和HSP 70的表达量较TTX组明显下降（P〈0.05）。HSP 70蛋白表达与p-STAT3蛋白表达呈正相关（r=0.826,P〈0.05）。经历缺血再灌注后,TTX组和TTX＋AG490组心肌细胞AI明显高于对照组（P〈0.05）;与TTX组相比,TTX＋AG490组AI显著增加（P〈0.05）。结论 JAK2/STAT3信号通路通过上调HSP 70的表达,调动心脏内源性保护机制,介导TTX心脏停搏液对缺血心肌的保护作用。     

尼可地尔超极化心脏停搏心肌保护剂量－效应关系的实验研究

目的 :对不同浓度尼可地尔心肌麻痹液超极化心脏停搏心肌保护的剂量 -效应关系进行研究 ,选择最适心肌保护剂量。　方法 :实验分 6组 ,即对照组 (去极化心脏停搏组 )、5种不同浓度 (2 5、5 0、10 0、12 5和 15 0 μm ol/L)尼可地尔超极化心脏停搏组。 4℃心肌麻痹液 (40 ml/kg)诱停离体鼠心 ,每隔 30 min重复灌注心肌麻痹液 (2 0 m l/kg) ,(15± 1)℃心脏停搏 12 0 m in后再灌注 ,离体心工作 30 min。记录心脏机械停搏时间、再灌注后心脏复跳情况、心功能恢复 (左室发展压、主动脉流量及左室压力微分 )、冠状循环灌注平均流量、心肌丙二醛 (MDA )含量、心肌超微结构的改变。　结果 :尼可地尔心肌麻痹液心肌保护呈类似抛物线形的剂量 -效应关系。尼可地尔浓度为 10 0μmol/L时 ,L VDP的恢复率最佳 ,心肌保护效果最好。　结论 :尼可地尔超极化心脏停搏心肌保护的最适心肌保护剂量为 10 0μm ol/ L。     

常温充氧晶体停搏液心肌保护作用的实验研究

采用离体鼠心工作模型，比较并评定了常温充氧晶体停搏液连续灌注和低温乏氧晶体停搏液间断灌注对心肌保护作用的效果。结果表明，常温充氧晶体停搏液能减少心肌细胞酶的漏出，加强心肌细胞内ＡＴＰ含量的储存，保护心肌细胞的超微结构，心肌保护效果明显优于低温乏氧晶体停搏液。     

木犀草素对冷保存不同时限大鼠心脏功能的影响

目的:研究木犀草素能否延长心脏停搏保存液(UW液)对离体大鼠心脏的低温保存时间。方法:将40只成年SD大鼠随机分成4组(n=10):冷保存12h对照组(12h-UW组)与实验组(12h-Lu组),冷保存18h对照组(18h-UW组)与实验组(18h-Lu组),利用Langendorff离体心脏灌流法,观察心脏在4℃含或不含木犀草素的UW液中保存12h或18h,复灌60min后心脏功能的变化,比较心功能指标:心率(HR)、左心室最大收缩压(LVPSP)、左心室压力变化率(±dp/dtm a x),心脏冠脉流量(CF)及冠脉流出液中磷酸肌酸激酶(CK)的释放量。结果:随着冷保存时间的延长,木犀草素能明显减缓离体大鼠心脏收缩功能(LVPSP,+dp/dtm a x)与舒张功能(-dp/dtm a x)的下降,增加冠脉流量,减少心肌酶CK的漏出,12h-UW组与12h-Lu组、18h-UW组与18-Lu组各观察指标相比差异均有统计学意义(P<0.05)。结论:木犀草素对长时间冷保存的离体大鼠心脏有明显的保护作用。     

外源性磷酸肌酸对未成熟心肌的保护作用

目的 探讨Ｓｔ．Ｔｈｏｍａｓ．Ⅱ心脏停搏液添加外源怀磷酸肌酸（ＣＰ）对未成熟心肌的保护效果,并观察其抗心律失常作用。方法 采用成熟心肌的保护效果,并观察其抗心律失常作用。方法 采用幼鼠（１８～２１ｄ）离体工作心模型,１４℃低温缺血１２０ｍｉｎ,缺血前主动脉根部灌注４℃ Ｓｔ．Ｔｈｏｍａｓ‘Ⅱ停博液（对照组）或Ｓｔ．Ｔｈｏｍａｓ’Ⅱ停搏液加４℃Ｓｔ．Ｔｈｏｍａｓ‘Ⅱ停博液ＣＰ＊（１０ｍｍｏｌ．Ｌ＾－     

脂质体携载前列腺素E1含血停搏液对未成熟心肌的保护效果

目的：探讨脂质体携载前列腺素E1(Lipo-PGEl)加入Thcmas Ⅱ停搏液对未成熟心肌的保护效果。方法：2～3周龄新西兰大白兔20只,随机分为2组,每组10只。建立Langendoff离体心脏灌注模型。对照组：TlxxnasⅡ号停搏液灌注加低温;实验组：Lipo-PGE1加入ThomasⅡ号停搏液灌注并行低温。全心平均停循环90min,再灌注30min。观察指标：冠脉流量恢复率(CFR)、心肌丙二醛(MDA)／超氧化物岐化酶(SOD)含量、心肌三磷酸腺苷ATP含量、心肌含水量、心肌磷酸肌酸激酶(CK)漏出量和乳酸脱氢酶(LDH)漏出量。结果：再灌注末实验组心肌MDA含量低于对照组,而SOD含量高于对照组;实验组CFR和再灌注末心肌ATP含量高于对照组;实验组心肌含水量、CK和LDH漏出量低于对照组。结论：Lipo-PGE1加入含血ThcmasⅡ号停搏液可改善对未成熟心肌的保护效果。     

Ischemic preconditioning in immature hearts： mechanism and compatibility with cardioplegia

Objective To investigate (1) whether ischemic preconditioning (IPC) could protect immature rabbit hearts against ischemia-reperfusion injury and (2) the role of K(ATP) channel in the mechanism of myocardial protection. Since cardioplegia is a traditional and effective cardioprotective measure in clinic, our study is also designed to probe the compatibility between IPC and cardioplegia. Methods New Zealand rabbits aged 14-21 days weighing 220-280 g were used. The animals were anesthetized and heparinized. The chest was opened and the heart was quickly removed for connection of the aorta via Langendorff’s method within 30 s after excision. All hearts were perfused with Krebs-Henseleit buffer balanced with gas mixture (O［２］∶CO(2)=95%∶5%) at 60 cm H［2O］ (perfusion pressure). IPC consisted of 5 min global ischemia plus 10 min reperfusion. Glibenclamide was used as the K(ATP) channel blocker at a concentration of 10 μmol/L before IPC. Cardiac arrest was induced with 4℃ St. Thomas cardioplegic solution, at which point the heart was made globally ischemic by withholding perfusion for 45 min followed by 40 min reperfusion. Thirty immature rabbit hearts were randomly divided into four groups: CON (n=9) was subjected to ischemia-reperfusion only; IPC (n=9) underwent IPC and ischemia-reperfusion; Gli (n=6) was given glibenclamide and ischemia-reperfusion; and Gli+IPC (n=6) underwent glibenclamide, IPC and ischemia-reperfusion. Coronary flow (CF), HR, left ventricle developed pressure (LVDP), and ±dp/dt(max) were monitored at equilibration (baseline value) and 5, 10, 20, 30 and 40 min after reperfusion. The values resulting from reperfusion were expressed as a percentage of their baseline values. Arrhythmia quantification, myocardial enzyme in the coronary effluent and myocardial energy metabolism were also determined. Results The recovery of CF, HR, LVDP and ±dp/dt(max) in preconditioned hearts was best among the four groups. The incidence of arrhythmia was low and less CK-MB leaked out in the IPC group. Myocardial ATP content was better preserved by IPC. Pretreatment with glibenclamide completely abolished the myocardial protection provided by IPC, but did not affect ischemia-reperfusion injury. Conclusions While applying cardioplegia, IPC provides significant cardioprotective effects. Activation of K(ATP) channels is involved in the mechanism of IPC-produced cardioprotection.     

Cardioprotective effects of mitochondrial KATP channels activated at different time

Backgroud Recent studies in adult hearts have indicated that KATP channels in the inner mitochondrial membrance are responsible for the protection. And we investigated whether opening of mitochondrial KATP channels (mKATP) could provide myocardial protection for immature rabbits and determined its role in cardioprotection.Methods Thirty-four 3-4-week-old rabbits, weighing 300-350 g, were divided randomly into five groups: Group Ⅰ (control group, n=8); Group Ⅱ ［diazoxide preconditioning group; n=8; the hearts were pretreated with 100 μmol/L diazoxide for 5 minutes followed by 10-minute wash out with Krebs-Henseleit buffer (KHB)］; Group Ⅲ ［diazoxide+5-hydroxydeconate (5-HD) preconditioning group; n=5; the hearts were pretreated with 100 μmol/L diazoxide and 100 μmol/L 5-HD); Group Ⅳ (diazoxide+cardioplegia group; n=8; cardioplegia containing 100 μmol/L diazoxide perfused the hearts for 5 minutes before ischemia); Group Ⅴ (diazoxide+5-HD+cardioplegia group; n=5; the cardioplegia contained 100 μmol/L diazoxide and 100 μmol/L 5-HD). All hearts were excised and connected to langendrff perfusion system and passively perfused with KHB at 38℃ under a pressure of 70 cmH2O. After reperfusion, the recovery rate of left ventricular diastolic pressure (LVDP), ±dp/dtmax, coronary flow (CF), the creatinine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST) in coronary sinus venous effluent and the tissue ATP were measured. Mitochondria were evaluated semiquantitatively by morphology.Results After ischemia and reperfusion (I/R), the two groups that were treated by diazoxide only (Groups Ⅱ and Ⅳ) had a significant improvement in LVDP, ±dp/dtmax, and CF recovery. AST, LDH, and CK were decreased, and the levels of tissue ATP in the two groups were higher. Mitochondria was protected better in Group Ⅳ than in other groups. Conclusions Activating mKATP channels before and during ischemia can similarly protect immature rabbit hearts, and the mechanism is related to the direct protective effect on mitochondria. Opening of mKATP channel during ischemia provides a better protection for mitochondria than it does before ischemia.     

不同浓度硝酸甘油对大鼠离体心脏保护8 h的效果

目的 探讨在托马斯液中加入不同浓度硝酸甘油对大鼠离体心脏保护8 h的效果。 方法 取30只Wistar大鼠,建立Langendorff离体心脏灌注模型,按保存液不同随机分为单纯托马斯液组、托马斯液+4×10-6 mol/L硝酸甘油组和托马斯液+4×10-5 mol/L硝酸甘油组,每组10只,比较4 ℃低温保存8 h后各组心脏功能指标;切取左心室壁组织于透射电镜下观察超微结构变化。 结果 4 ℃低温保存8 h后,与单纯托马斯液组相比,托马斯液+4×10-5 mol/L硝酸甘油组的心功能显著改善,细胞超微结构受损较轻;而托马斯液+4×10-6 mol/L硝酸甘油组各指标则无显著改善。 结论 在托马斯液中加入4×10-5 mol/L硝酸甘油可显著提高大鼠离体心脏的保存效果。     

Protective effects of pinacidil hyperpolarizing cardioplegia on myocardial ischemia reperfusion injury by mitochondrial KATP channels

Background  Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels (K_ATP) were the end effectors of cardio-protection. But whether mitochondrial K_ATP plays an important role in hyperpolarizing cardioplegia is not apparent. The present study investigated the effect of hyperpolarizing cardioplegia containing pinacidil (a nonselective K_ATP opener) on ischemia/reperfusion injury in rat hearts, especially the role of mitochondrial K_ATP in pinacidil hyperpolarizing cardioplegia.

Methods  Sprague-Dawley rat hearts were Langendorff-perfused for 20 minutes with Krebs-Henseleit buffer at 37°C before equilibration. Cardiac arrest was then induced in different treatments: there was no arrest and ischemia in the normal group, the control group were arrested by clamping the aorta, depolarizing caidioplegia (St. Thomas solution containing 16 mmol/L KCl) and hyperpolarizing cardioplegia groups used St. Thomas solution containing 0.05 mmol/L pinacidil and 5 mmol/L KCl to induce cardiac arrest in group hyperkalemic and group pinacidil, in group hyperkalemic + 5-hydroxydecanote (5HD) and Pinacidil + 5HD, 5HD (0.1 mmol/L) was added to the above two solutions to block mitochondria K_ATP channels. Global ischemia was then administrated for 40 minutes at 37°C, followed by 30 minutes of reperfusion. At the end of equilibration and reperfusion, hemodynamics, ultrastructure, and mitochondrial function were measured.

Results  In the control group, ischemia/reperfusion decreased the left ventricular developed pressure, heart rate, coronary flow, mitochondrial membrane potential, impaired mitochondrial respiratory function, increased reactive oxygen species and left ventricular end diastolic pressure. Damage to myocardial ultrastructure was also evident. Both depolarized arrest and especially hyperpolarized cardioplegia significantly reduced these lesions. 5HD partially blocked the beneficial effects of pinacidil cardioplegia but showing no effects on hyperkalemic arrest.

Conclusions  Pinacidil cardioplegia provides better cardioprotection with preservation of hemodynamics, ultrastructure, and mitochondrial function than traditional cardioplegia. The mitochondria K_ATP channels may play an important role in the protection mechanism.

     

低温室颤法心内直视手术的临床效果观

目的观察与评价低温室颤法在心内直视手术中心肌保护的临床效果.方法将24例先天性心脏病病人随机分为冷心脏停搏液组(n=13)和低温室颤组(n=11),分别行心内直视畸形纠治术,观察心肺转流(CPB)时间、辅助通气时间、心律失常发生率、多巴胺使用率、循环指标、血气分析指标、ICU恢复时间等指标.结果冷心脏停搏液法的术中CPB时间、辅助通气时间、多巴胺使用量多于低温室颤组;心律失常率、循环指标、血气分析指标、ICU恢复时间等两组无差异.结论低温室颤法不存在心肌缺血和缺血再灌注损伤,是一种可供选择的安全、有效的良好心肌保护方法.     

缺血后处理对不同时程冷保存大鼠心脏的作用研究

目的:研究缺血后处理(postconditioning)对不同时程冷保存大鼠心脏的作用及其机制。方法:利用Langendorff离体鼠心灌注法,观察大鼠心脏在Celsior液(4℃)中保存3 h或5 h后,在其后复灌60 min期间血流动力学的恢复情况,并对复灌期间心律失常严重程度进行定量分析。缺血后处理采用全心停灌30 s,复灌30 s,循环3次。结果:(1)与3 h冷保存对照组相比,大鼠心脏冷保存3 h后给予缺血后处理,在多个复灌时间点上可明显降低左室舒张末期压力,而心率、左室发展压、左室最大收缩/舒张速率、冠脉流出量、心率与发展压的乘积等的恢复率在复灌期明显高于3h对照组。心脏冷保存3 h后心律失常的发生率在复灌第0~10min时最高,缺血后处理可明显降低心律失常的发生率。(2)在缺血后处理短暂复灌期的K-H灌流液中加入100μmol/L的5-HD(线粒体ATP依赖性钾离子通道的阻断剂),可取消缺血后处理降低左室舒张末期压力,增高心率、左室发展压、左室最大收缩/舒张速率、冠脉流出量、心率与发展压乘积的作用。心律失常评分亦明显高于3 h缺血后处理组。(3)大鼠心脏冷保存5 h后给予缺血后处理,在复灌期间各项动力学指标以及心律失常评分上与5 h冷保存对照组无明显差异。结论:缺血后处理对于3 h冷保存的大鼠心脏有显著的保护作用,其作用机制可能是部分通过激活线粒体ATP依赖性钾离子通道起作用,而缺血后处理对于5 h冷保存的大鼠心脏并无保护作用。     

外源性磷酸肌酸对大鼠供心保存的保护作用

目的：观察外源性磷酸肌酸对大鼠供心保存效果及其保护机制。方法：40只健康雄性SD大鼠随机均分A、B2组，移植前供心保存240min，A组供心用4℃St.Thomas液保存。B组保存液中添加外源性磷酸肌酸。保存后进行腹腔异位心脏移植术，并观察供心复跳情况。24h后处死受体动物，切除移植心脏，测心肌组织中脂质过氧化物（LPO）、超氧化物歧化酶（SOD）、三磷酸腺甘（ATP）含量，电镜观察心肌超微结构改。结果：B组移植心脏自动复跳率高于A组，心律失常发生率低于A组。B组心肌组织中SOD、ATP含量均高于A组（P＜0.05），LPO含量低于A组（P＜0.01），心肌超微结构损伤较A组轻。结论：外源性磷酸肌酸能明显增强保存液对心脏保护作用，其机制可能与其对线粒体结构保护良好减少自由基产生有关。