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.     

不同浓度硝酸甘油对大鼠离体心脏缺血/再灌注损伤的作用

目的:探讨不同浓度硝酸甘油(nitroglycerin,GTN)对大鼠离体心脏缺血/再灌注损伤的作用。方法:采用离体大鼠心脏Langendorff灌流方法,结扎冠状动脉左前降支30 min和再灌注120 min复制局部缺血/再灌注损伤模型,测定各项心室动力学指标、冠状动脉流出液中乳酸脱氢酶(lactatede hydrogenase,LDH)含量及心肌梗死面积。结果:与单纯缺血/再灌注组相比,GTN高浓度组(2×10-6mol/L)抑制了再灌注后心功能的恢复(P<0.05~P<0.01),增大了心肌梗死面积(P<0.01),再灌注时冠状动脉流出液中LDH释放增加(P<0.05);GTN中浓度组(1×10-7mol/L)与单纯缺血/再灌注组相比,对心功能的恢复、心肌梗死面积和LDH含量改变不明显;GTN低浓度组(1×10-8mol/L)明显促进了再灌注后心功能的恢复,减小了心肌梗死面积,冠状动脉流出液中LDH释放减少(P<0.05~P<0.01)。结论:高浓度GTN加重心肌缺血/再灌注损伤,中浓度GTN对缺血/再灌注心肌作用不明显,低浓度GTN可保护缺血/再灌注心肌。     

卡托普利心麻液对离体心脏的保存作用

２０只健康家兔随机分为对照组和卡托普利组，每组１０只，采用Ｌａｎｇｅｎｄｏｒｆｆ灌注兔心模型。对照组单纯用圣托马斯液作为心停跳液和保存液，卡托普利组则在圣托马期液中加入卡托普利。离体以及于４℃下缺血停跳６ｈ，再灌注３０ｍｉｎ。结果：卡托普利组缺血后心输出量，心肌肌酸磷磷激酶含量，超氧化物歧化酶活性，过氧化脂质含量及六酮２前列腺素含量分别为（３２．４±２．６）ｍｌ／ｍｉｎ，（１８３．５±７．８）Ｕ／     

硝酸甘油对离体大鼠心脏心肌缺血-再灌注损伤的作用研究

目的：探讨硝酸甘油（NTG）对离体大鼠心脏缺血期补充一氧化氮（NO）供体对缺血-再灌注损伤的影响。方法：取36只大鼠建立Langendorff离体心脏灌流模型,离体大鼠心脏缺血30min,再灌注60min,分为用药组（18只）及对照组（18只）。用药组于缺血期给予4.4×10-3mmol/L硝酸甘油,碳酸氢盐缓冲液灌注。对照组仅给予碳酸氢盐缓冲液灌注。全部心脏均测定NO释放量、肌酸激酶漏出量及（或）心脏功能。结果：用药组大鼠心脏使用NTG后表现为两种效应。其中,非心室颤动组10只,NTG增加肌酸激酶漏出量,减弱再灌注期心脏功能的恢复,伴随缺血期NO释放量的增加;心室颤动组8只,NTG减少肌酸激酶的释放,但心脏于再灌注期持续心室颤动,缺血期NO释放量无明显增加。结论：缺血期给予同一剂量NTG对心肌缺血-再灌注损伤产生双重效应,既可增加心肌损伤,又可减轻心肌损伤。     

离体心脏9 h心脏移植早期结果

供心保护仍是限制心脏移植广泛开展的重要因素,常规灌注保存超过5 h的心脏是移植失败的重要因素之一.2005年3月,我院施行1例同种异体原位心脏移植手术,供心缺血时间超过常规时限,但术后近期效果良好,现报告如下.     

腺苷预处理对大鼠离体心脏长期保存的心肌保护作用

目的观察腺苷预处理对大鼠离体心脏长期保存的心肌保护作用。方法将24只健康雄性SD大鼠随机分为4组,每组6只,分成空白对照组、预处理组、保存组和预处理后保存组。离体大鼠心脏用Langendorff装置灌注稳定后,分别给予腺苷预处理后再灌注、心脏保存24 h后再灌注及腺苷预处理后再经24 h保存后再灌注60min,观察左室收缩功能的恢复率、冠脉回流液中肌酸肝激酶(creatine kinase,CK)、乳酸脱氢酶(lactate dehydrogenage,LDH)的浓度以及心肌形态结构改变。结果预处理组同空白对照组相比,各项指标差异无显著性(P>0.05)。单纯保存组同对照组相比,左室收缩功能明显减弱,冠脉回流液中心肌酶的漏出明显增加,光镜及电镜观察心肌损伤严重。而经腺苷预处理后再保存组,左室收缩功能的恢复率较单纯保存组有明显提高52.1%±7.4%vs35.9%±4.8%,P<0.05,心肌酶漏出明显减少[CK:(302±42)IU/Lvs(632±118)IU/L;LDH:(28±8)IU/Lvs(78±11)IU/L,P<0.05],光镜及电镜观察,心肌损伤程度明显减轻。结论腺苷预处理过程本身对心肌细胞无明显损伤,是比较安全的;腺苷预处理对离体心脏长期保存有明显的保护作用。     

硫化氢对大鼠离体心脏低温保存效果的实验研究

目的 观察硫化氢（H2S）对大鼠离体心脏的保护作用。方法 将48只SD大鼠随机分成对照组（ST组）和实验组（HST组）,每组24只,分别采用St.ThomasⅡ液和St.ThomasⅡ液＋H2S为停搏液及保存液,保存心脏4 h,6 h,8 h。采用Langendorff心脏灌注和工作模型装置进行心脏保存前及保存后再灌注30 min心功能测定,比较心功能恢复率、心肌含水量、心肌酶[乳酸脱氢酶（LDH）及磷酸肌酸激酶（CK）]漏出量以及心肌组织超微结构变化。结果 保存4 h、6 h后,HST组心功能指标及心肌含水量与ST组差别无统计学意义,但心肌酶漏出量明显减少;保存8 h后HST组所测各指标均优于ST组。结论 加入H2S的St.ThomasⅡ液可以提高大鼠离体心脏的保存效果。     

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.     

蛋白激酶C对离体兔心脏的保护作用

目的探讨蛋白激酶C对离体兔心的保护及机制。方法应用蛋白激酶C的激活剂和阻断剂,通过Langendroff离体兔心灌注模型,测定心功能指标、心肌CK-MB、LDH、MDA、SOD含量,计算心肌含水量及检测凋亡细胞,了解蛋白激酶C对心功能的影响。结果缺血预适应组和蛋白激酶C激活组的心肌CK-MB(233·6U/g±24·6U/g,285·9U/g±21·4U/g),LDH(83·9U/g±6·5U/g,91·2U/g±5·4U/g和SOD(201·0U/g±17·4U/g,91·9U/g±22·1U/g)含量均高于对照组(132·5U/g±24·8U/g,74·1U/g±7·4U/g,180·3U/g±16·8U/g)和激活阻断组(135·1U/g±28·8U/g;75·1U/g±8·8U/g,184·5U/g±16·9U/g)(P<0·05),而MDA含量、心肌含水量明显低于对照组和激活阻断组(均P<0·05)。结论蛋白激酶C对离体兔心具有肯定的保护作用。     

同种原位心脏移植供心的保护

0　引言　心脏移植是治疗终未期心脏病唯一可行的方法,2000-01-26我科成功完成1例同种异体原位心脏移植术,存活至今,心功能及生活质量良好,就供心心肌保护及体会报告如下.1　临床资料　供心系脑死亡男性患者,27岁,术前已建立有效人工辅助呼吸.以3mg.kg-1肝素iv,快速胸部正中入路剖胸,倒“T”剪开心包,心包内置冰水降温;升主动脉根部插入灌注管,近隔肌横断下腔静脉;随即阻闭升主动脉,经冷灌管注入4℃改良St.Thomas停搏液1500mL,灌注压力7～8kPa,同时横断右侧肺静脉使左室减压,左手托起心脏于左右侧肺静脉上下缘分置4根标记线,然后切断左肺…     

Propofol improves cardiac functional recovery after ischemia-reperfusion by upregulating nitric oxide synthase activity in the isolated rat hearts

Background There are few studies to assess whether propofol attenuates myocardial ischemia-reperfusion injury via a mechanism related to nitric oxide （NO） route, so we designed this randomized blinded experiment to observe the changes of NO contents, nitric oxide synthase （NOS） activity, NOS contents in the myocardium, and cardiac function in ischemic reperfused isolated rat hearts, and to assess the relation between myocardial NO system and cardioprotection of propofol. Methods The hearts of 30 Sprague-Dawley male rats were removed, mounted on a Langendorff apparatus, and randomly assigned to one of three groups （n=10 each group） to be treated with the following treatments in a blinded manner： Group 1, control group, after perfusion with pure Krebs Henseleit bicarbonate （K-HBB） buffer solution for 15 minutes, hearts were subjected to 20 minutes global ischemia followed by 60 minutes reperfusion with pure K-HBB buffer; Group 2, after perfusion with K-HBB buffer solution containing propofol （10 ug/ml） for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution; Group 3, after perfusion with K-HBB buffer solution containing propofol （10ug/ml） and L-NAME （100 umol/L） for 15 minutes, the hearts underwent 20 minutes global ischemia followed by 60 minutes reperfusion with the same K-HBB buffer solution. The cardiac function was continuously monitored throughout the experiment. The coronary flow was also measured. An ISO-NO electrode was placed into the right atrium close to the coronary sinus to continuously measure NO concentration in the coronary effluent. The tissue samples from apex of hearts in Groups 1 and 2 were obtained to measure the NOS activity by spectrophotometry and the NOS contents by immunohistochemistry, respectively. Results The cardiac function was significantly inhibited after ischemia and then gradually improved with reperfusion in all three groups. As compared with Group 1, the cardiac function variables and coronary flow at all the observed points were significantly improved in Group 2. The cardiac function variables and coronary flow were better in Group 3 than in Group 1, but were inferior in Group 3 than in Group 2. Both NO contents and NOS activity in the myocardium were significantly higher in Group 2 than in Group 1. However, NOS contents in the myocardium did not significantly differ between Groups 1 and 2. Conclusions In isolated rat hearts, propofol can improve cardiac functional recovery after ischemia-reperfusion by upregulating NOS activity in the myocardium. The NO system may play an important role in the preservation of myocardial ischemia-reperfusion injury produced by propofol.     

心脏移植患者围手术期心肌肌钙蛋白Ⅰ的动态变化

目的观察心脏移植患者围手术期心肌肌钙蛋白Ⅰ(CTn Ⅰ)的动态变化,了解心脏移植中心肌保护的效果及术后心脏损伤恢复的情况.方法测定5例心脏移植患者术前、手术当日及术后(1～17)天心肌肌钙蛋白Ⅰ的变化.供心植入前采用St.Thomas液保护,植入中用冷血保护.结果心脏移植患者与供者术前CTn Ⅰ基本在正常范围,手术当日及术后CTn Ⅰ较术前升高,然后逐渐下降,于第12天恢复在正常值范围内.第2例患者停机后对鱼精蛋白过敏又二次转流,术后CTn Ⅰ较其他4例患者峰值高且下降速度慢,于术后第21天死于脏器衰竭,另4例患痊愈出院.结论心肌肌钙蛋白Ⅰ在心脏移植当日及术后明显高正常值,术后第12天基本正常水平.心肌肌钙蛋白Ⅰ明显升高也表明供心的心肌保护仍存在着缺陷.     

低温氧合血+Celsior液微流量持续灌注对大鼠右心的保护效果

目的 探讨低温氧合血+Celsior液微流量持续灌注对大鼠右心的保护效果.方法 Wistar大鼠切取全心,随机分为3组,实验组的心脏以4℃氧合血+Celsior液微流量(1 mL/h)持续灌注低温保存4 h;对照组以4℃Celsior液微流量持续灌注低温保存4 h;单纯冷保存组以4℃Celsior液单纯浸泡保存4 h.保存后的鼠心用Langen-dorff装置灌注,切除右心耳,将一球囊放入右心室.测定右心室血流动力学指标;高效液相色谱仪测定ATP含量;光镜和电镜观察心肌组织的形态学改变.结果 灌注30 min时,实验组的右心室收缩压(RVSP)为(26.64±3.3)mmHg,右室舒张压(RVDP)为(19.07±3.23)mmHg,右心室压力微分(±dp/dt)为(752±77)mmH/s;对照组的RVSP为(23.98±4.02)mmHg,RVDP为(11.31±2.46)mmHg,±dp/dt为(548±103)mmHg/s;单纯冷保存组的RVSP为(22.38±3.65)mmHg,RVDP为(9.43±2.44)mmHg,±dp/dt为(457±151)mmHg/s,实验组的血流动力学指标优于对照组和单纯冷保存组(P<0.05).实验组心肌细胞的ATP含量为(1.225±0.316)μmol/L,对照组为(0.852±0.303)μmol/L,单纯冷冻保存组为(0.587±0.232)μmol/L,实验组ATP含量明显高于对照组和单纯冷保存组(P<0.05).实验组的组织学损害轻于对照组和单纯冷保存组.结论 低温氧合血+Celsior液微流量持续灌注对大鼠右心有保护效果.     

Cardioprotective Effects of Melatonin on Recovery of Rat Donor Hearts after 12-Hour Preservation

Hearttransplantationisanacceptedtherapeuticmodalityforselectpatientswithend stageheartdis ease .However ,the“safe”ischemictimeforcardiacallograftsinclinicalpracticeisstilllimitedto 4to 6h .Thislimitationgreatlyexacerbatesthecriticalshortageofdonororgansandprecludeslong distanceorganprocurementandsharing .Furthermore ,inade quatemyocardialpreservationcontinuestobeasignif icantcauseofearlygraftfailureandrecipientmortali ty[1] .Thekeytoextendingthesafeischemictimeofcardiacallograftsistheelucida…     

Comparative Study on the Effects of Self-made Liver Preservation Solution on Secretion of ICAM-1 and NO in Rats

In order to study the effect of self-made liver preservation solution on liver preservation by comparing with UW solution and HC-A solution, the self-made liver preservation solution （SM） and perfusion solution were prepared under the aseptic conditions. The isolated non-circulated perfusion rat liver model was established. According to the different preservation solutions, the rats were randomly divided into UW group, SM group and HC-A group. The three groups were divided into 6 subgroups according to the preservation duration （n=6 in each group）. The transferase in liver perfusion solution and intercellular adhesion molecule-1 （ICAM-1） and nitric oxide （NO） in liver tissues were determined at 2, 8 and 24 h respectively. The results showed that the levels of alanine aminotransferase （ALT） and aspartate aminotransferase （AST） had no significant difference between SM group and UW group, but significantly lower than in HC-A group. The levels of ICAM-1 and NO were increased simultaneously in SM group and UW group （P〉0.05）, but there was significant difference as compared with HC-A group （P〈0.05）. At the same time point, the level of ICAM-1 was higher in SM group than in UW group, but NO was lower. The preservation effect of SM solution is the same as UW solution, but better than HC-A solution.     

心先安对缺血预处理心肌保护作用的影响

目的探讨缺血预处理对缺血-再灌注心肌的保护作用及心先安干预的影响。方法32只雄性新西兰大耳白兔,在冠状动脉左室支的上3/4~4/5处穿以丝线,造成心肌缺血再灌注(MIR),随机分为四组:MIR组、心先安+MIR组(MCA+MIR)、缺血预处理IP+MIR组(IP+MIR)、心先安+IP+MIR组(MCA+IP+MIR)。实验结束后测定血浆中内皮素(ET)、心钠素(ANP)和血清肌酸肌酶(CK)的含量,分析心肌梗死范围。结果(1)血浆ET浓度,MIR组和MCA+MIR组分别为67.15±5.10 pg.ml-1和58.44±3.47pg.ml-1(P<0.01);IP+MIR组和MCA+IP+MIR组分别为58.94±3.16 pg.ml-1和53.14±3.24 pg.ml-1(P<0.01)。(2)血浆ANP浓度,MIR组和MCA+MIR组分别为910.09±112.29pg.ml-1和955.33±106.06 pg.ml-1(P>0.05);IP+MIR组和MCA+IP+MIR组分别为1356.18±93.41 pg.ml-1和1402.43±138.78 pg.ml-1(P>0.05),但较MIR组和MCA+MIR组明显增加(P<0.01)。(3)血清CK浓度,MCA+MIR组和IP+MIR的分别为177.25±31.04 mmol.L-1和169.25±31.37 mmol.L-1(P>0.05),明显低于MIR组(554.00±148.62 mmol.L-1)(P<0.01);MCA+IP+MIR组为105.00±13.18 mmol.L-1,明显低于其他组(P<0.01);(4)心肌梗塞范围,MCA+MIR组和IP+MIR组分别为21.13±1.78%和21.58±2.22%,(P<0.05),明显低MIR组32.85±3.18%(P<0.01);MCA+IP+MIR组为13.69±1.01%,较其他组明显减少(P<0.01)。结论(1)IP可使MIR过程中ET、CK浓度和ANP浓度增高,并减少MIR所致的心肌坏死。(2)MCA可降低MIR血浆中ET和CK浓度,并减少MIR所致的心肌坏死。(3)MCA能加强IP降低MIR对血清CK浓度的作用。