速水对改善供心保存的作用

目的 研究在冷缺血期供心保存液中速尿对改善鼠心保存效果的影响。方法 Ｓｔ．Ｔｈｏｍａｓ液中加入速尿停搏并冷保存大鼠心脏６小时，利用离体鼠心非循环Ｌａｎｇｅｎｄｏｒｆｆ灌流功能测定模型，测定心脏功能的恢复，检测心肌细胞ＡＴ客ＴＡＮ的含量等，结果 加速尿组保存后的左心功能恢复明显优于不加速尿组，加速尿组保存后心肌细胞ＡＴ客ＴＡ怕恢复率明显高于不加速尿组。结论保存液中的速尿能改善供心的保护效果。     

前列腺素E1改善离体鼠心保存效果的研究

目的　探讨在冷缺血期供者心脏保存液中前列腺素 Ｅ１（ｐｒｏｓｔａｇｌａｎｄｉｎ Ｅ１）对改善鼠心的保存效果。　方法　将１４ 只大白鼠随机分为对照组和实验组，每组７ 只。对照组用 Ｓｔ Ｔｈｏｍ ａｓ停搏液停搏并保存大鼠心脏６ 小时；实验组在 Ｓｔ Ｔｈｏｍ ａｓ液中加入前列腺素 Ｅ１（５ μｇ／ Ｌ）停搏并冷保存６ 小时，利用离体鼠心非循环式 Ｌａｎｇｅｎｄｏｒｆｆ 灌流功能测定模型，测定左心室舒张期末压（ Ｌ Ｖ Ｅ Ｄ Ｐ）、左心室发展压（ Ｌ Ｖ Ｄ Ｐ）和左心室压力变化率（＋ ｄｐ／ｄｔ），并检测心肌细胞线粒体三磷酸腺苷（ Ａ Ｔ Ｐ）、腺嘌呤核苷酸总量（ Ｔ Ａ Ｎ）。　结果　实验组保存后的左心功能恢复明显优于对照组（ Ｐ＜ ０．０５），实验组保存后心肌细胞三磷酸腺苷和腺嘌呤核苷酸总量的浓度明显高于对照组（ Ｐ＜ ０．０５）。　结论　供者心脏停搏液和保存液中的前列腺素 Ｅ１ 能改善供心的保护效果。     

HOE-642联合改良K/Mg冷血心麻液对犬供心的保护作用

目的探讨HOE-642联合改良K／Mg冷血心麻液提高犬供心的保存效果的作用。方法雄性成年杂种家犬32只，随机分为整合组和常规组（每组16只，供、受者各8只）。（1）整合组：供心保护采用HOE-642联合改良K／Mg冷血心麻液的“整合策略”；（2）常规组：供心保护采用临床上常规方法。所有动物的供心均冷浸浴保存4h，心脏移植用原位标准法。记录不同时段的心功能指标；实验结束后观察心肌超微结构并测定心肌含水量。结果每组各1例主动脉开放后因主动脉吻合口漏血，失血陛休克死亡，剔除出实验；其余动物均成功脱离体外循环。整合组的移植心脏左心室收缩功能和舒张功能恢复指标显著优于常规组（P〈0．05）；整合组心肌组织含水量显著小于常规组（P〈0．05）；整合组心肌细胞亚细胞结构的保存亦优于常规组。结论临床常规方法和HOE-642联合改良K／Mg冷血心麻液的“整合策略”，均可安全冷保存供心4h，但后者能进一步减轻心肌水肿、维持心肌细胞结构完整、促进缺血／再灌注损伤后心功能的恢复，具有更佳的心肌保护效果。     

Fas/FasL和Caspase-3在二氮嗪强化Celsior液超时冷保存鼠心移植中的表达及其意义

研究心肌线粒体三磷腺苷敏感性钾离子通道(mitochondrial ATP-sensitive potassium channel,MitoKATPC)开放剂二氮嗪(diazoxide,DE)添加入Celsior液中对大鼠供心超时冷保存的效果,并探讨其抗心肌凋亡作用的可能机制.方法 SD大鼠112 只,随机分成7组,每组16只(供者、受者各8只).(1)Celsior组:保存液为单纯Celsior液;(2)DE组:保存液为30 μmol/L DE+Celsior 液;上述两组又以保存时间不同分为5 h、8 h、10 h组.(3)5-HD组:保存液为Celsior液+DE (30 μmol/L)+5-HD(100 μmol/L),保存时间为5 h.利用改良Heron法建立大鼠颈部异位心脏移植模型,观察移植术后5 min内心脏恢复跳动、心率表现;采用原位末端标记染色法检测心肌细胞凋亡,用免疫组织化学方法检测心肌Fas/FasL和Caspase-3蛋白的表达情况;以及用电镜观察心肌超微结构等.结果 (1)除5 h保存时间的心脏外,DE各组心脏移植术后30 s复跳率较相应Celsior液组显著提高;DE组心率明显较Celsior液组快(P<0.05),DE 10 h组与Celsior 5 h组无明显区别(P>0.05);(2)与Celsior液组相比,DE处理明显降低各组心肌细胞凋亡指数(P<0.05),减少Fas/FasL和Caspase-3蛋白的表达(均为P<0.05);DE 10 h组与Celsior 5 h组各指标比较差异无统计学意义(P>0.05);(3)5-HD可取消上述DE的作用;(4)DE各组和Celsior 5 h组心肌超微结构保护相对较佳:肌纤维排列整齐,肌节清,线粒体肿胀不明显,嵴结构较为清楚;Celsior 10 h组心肌结构尚清楚,但肌纤维疏松,个别区域肌丝肌节溶解,线粒体肿胀较明显,嵴模糊.结论 DE强化Celsior液冷保存的鼠供心,可能通过激活MitoKATPC,明显抑制Fas/FasL和Caspase-3蛋白的表达,保护线粒体功能和结构的完整,从而使心肌细胞凋亡减少,减轻缺血再灌注损伤,使得DE强化Celsior液超时(10 h)冷保存的鼠供心移植安全有效.     

二氮嗪改善供心超时冷保存效果的实验研究

目的　研究二氮嗪在离体大鼠心脏冷保存中的作用,探讨线粒体ATP敏感性钾通道(Mito chondrialATP sensitivepotassiumchannel,MitoKATPC)开放剂在改善供心功能中的可能机制,及超时(超过公认5h)冷保存供心的有效性。方法　SD大鼠随机分7组。对照组、二氮嗪(DE)组,以上两组又各分为冷保存3、5、10h组和DE +5 羟基葵酸盐(5 HD)组。采用Langendorff离体鼠心灌注法,复灌6 0min ,观察心脏血流动力学、冠脉流出液心肌酶漏出量及心肌水含量变化,并做心肌超微结构检查。结果　(1)冷保存3、5、10h后,DE组LVDP、±dp/dtmax、CF恢复率在多个复灌时间点上均优于对照组,且心肌酶漏出量明显减少。(2 )5、10h保存组中,DE处理后LVEDP的变化明显小于对照组。(3)与对照组相比,保存10h后DE组的心肌水含量明显降低,且心肌超微结构优于对照组。(4)与保存5h对照组相比,保存10h后DE组在复灌期可显著抑制LVEDP的增高;仅LVDP和-dp/dtmax恢复率较保存5h对照组低。(5 )DE的上述作用可被Mi-toKATPC的特异性阻断剂5 HD抵消。结论　Celsior保存液中加入DE能明显改善离体大鼠心脏冷保存效果,且供心的冷缺血安全时间可安全延长至10h,其保护机制涉及MitoKATPC的开放     

氨基酸盐温血停搏液诱导与末次灌注心肌的保护作用

采用离体大鼠工作心模型，以含谷氨酸和天门冬氨酸盐各１３ｍｍｏｌ／Ｌ的温血停搏液诱导与末次灌注行心肌保护研究，并与未用氨基酸盐以及单纯冷晶体停搏液进行比较。结果显示应用氨基酸盐可促进心脏功能恢复，明显改善复灌后心肌的氧代谢，心肌ＡＴＰ含量增加而含水量减少，超微结构改变轻，心肌保护效果显著优于未用氨基酸盐组和冷晶体停搏液组。     

前列腺素E1改善离体离心保存效果的研究

目的 探讨在冷缺血期供者心脏保存液中前列腺素Ｅ１对改善鼠心的保存效果。方法 将１４只大白鼠随机分为对照组和实验组，每组７只。对照组用ＳｔＴｈｏｍａｓ停搏液停搏并保存大鼠心脏６小时，实验组在ＳｔＴｈｏｍａｓ液中加入前列腺素Ｅ１（５μｇ／Ｌ）停搏并冷保存６小时，利用离体鼠心非循环式Ｌａｎｇｅｎｄｏｒｆｆ灌流功能测定模型，测定左心室舒张期末压（ＬＶＥＤＰ）、左心室发展压（ＬＶＤＰ）和左心室压力变化率（｜     

供体进食状况对大鼠供肝冷保存损伤的影响

探讨供体进食状况对大鼠供肝冷保存损伤的影响。方法健康的雄性ＳＤ大鼠１６只随机分为食组和禁食组。大鼠肝脏以高渗枸橼酸盐嘌呤液４℃冷保存２４小时，测定保存前后肝组织糖原、蛋白质、丙二醛的含量，超氧化物歧化酶（ＳＯＤ）和ＡＴＰ酶活性。结果：（１）进食能明显提升肝脏的糖尿原含量，肝脏冷保存后糖原含量均有显著下降。（２）饮食因素在短期内并未明显影响到肝脏的蛋白质代谢，冷保存对肝脏的蛋白质代谢亦未见明显影响。     

抑肽酶心肌保护机制的探讨

目的 探讨抑肽酶增强Ｓｔ．ＴｈｏｍａｓⅡ停跳液心肌保护作用的机制。方法 用离体豚鼠工作心脏模型，研究４℃、３３℃下不同剂量抑肽酶增强Ｓｔ．ＴｈｏｍａｓⅡ型跳液心肌保护效果，记录停跳前后心脏血流动力学和心肌酶学。结果 在４℃下抑肽酶能增加复灌后心肌ＡＴＰ的保存量，并存在剂量依赖关系；同时性马抑肽酶能明显减少保存后心肌酶的释放、并改善保存后心肌的超微结构；但抑肽酶组停跳后的心功能，较对照组无明显提高；     

二氮嗪心脏停搏液对供心的保护作用

目的探讨二氮嗪(diazoxide)心脏停搏液对冷保存供心细胞凋亡的作用。方法用单纯随机抽样法将32只新西兰大耳白兔随机分成4组(每组8只):二氮嗪组(KH液加入50μmol/L二氮嗪),STH组(St.Thomas液),5-HD组(KH液中加入50μmol/L二氮嗪和100μmol/L 5-hydroxydecanoic acid)和KH组(KH液)。兔心分别在相应的心脏停搏液中冷保存(4℃)6h,应用Langendorff灌注模型,在保存前后测左心室发展压(LVDP)、左心室内压上升最大速率(+dp/dtmax),以保存前LVDP、+dp/dtmax值作基数计算保存后的恢复率。用原位末端标记法(TUNEL)检测保存后心肌细胞凋亡,测定保存后心肌组织中三磷酸腺苷(ATP)、丙二醛(MDA)的含量。结果二氮嗪组的LVDP、+dp/dtmax恢复率和心肌组织中ATP含量明显高于其他3组(P<0.05),而心肌细胞凋亡率、心肌MDA含量均明显低于其他3组(P<0.05)。结论二氮嗪心脏停搏液对离体心脏有保护作用,其作用可能与线粒体钾通道(mitochondrial KATP)开放有关;线粒体钾通道阻滞剂5-HD可取消二氮嗪的心肌保护作用。     

含磷酸肌酸心脏停搏液对鼠供心的心肌保护作用

目的探讨含磷酸肌酸的心脏停搏液对离体心脏的保存效果，以延长供体心脏缺血的保存时间，提高心脏移植的效果。方法将20只Wistar大鼠随机分成两组，对照组（n=10）：使用冷晶体St．ThomasⅡ心脏停搏液灌注保护供心；实验组（n-10）：灌注含磷酸肌酸钠（2．5g／L）的冷晶体St．ThomasⅡ心脏停搏液保护供心。鼠心于低温保存4h后取心肌组织，测定心肌组织中三磷酸腺苷（ATP）含量和超氧化物歧化酶（SOD）活性。在光学显微镜和电子显微镜下观察心肌组织结构变化及线粒体水肿情况。结果供心冷藏保存4h后，实验组心肌组织中ATP含量明显高于对照组（2．75±0．99μmol／mg vs．1．77±0．86μmol／mg，P〈0．05）；SOD活性明显高于对照组（49．6±2．52U／mg vs．45．27±2．21U／mg，P〈0．05）。电子显微镜下观察：对照组心肌细胞核固缩，核膜内染色质凝聚、溶解，线粒体嵴间隙消失，间质血管内皮坏死；实验组心肌细胞核位于中心区，肌节各带结构清晰，肌质网扩张，闰盘各带连接结构清晰。结论含磷酸肌酸的心脏停搏液能明显增强供心的心肌保护作用。     

药物预处理与诱导超极化对离体心脏的保护研究

目的：探讨AT敏感性钾通道开放剂（KCOs)吡那地尔对Langendorff灌注兔心脏模型药物预处理与药物诱导超极化停跳的保护作用。方法：离体兔心40个,随机等分5组。对比研究2种浓度吡那地尔在4℃或37℃全心缺血40min,复灌20min的心肌组织腺苷酸含量,脂质过氧化物的变化,以及再灌注后10、20min心功能恢复的情况。结果（1）心脏诱导停跳以4℃超极化与药物预处理组迅速,37℃超极化组较为缓慢;再灌注后仅对照组心脏复跳较慢。（2）与对照组同期比较,比吡那地尔预处理以及超极化的心脏再灌注后心肌收缩力与左心室内压恢复较快,其中心肌收缩力的恢复更为显著;（3）再灌注后,对照组心肌ATP、总腺苷量、细胞能荷水平低于预处理与超极化组（P＜0．05或0．01）其中以37℃预处理ATP含量较高,而经吡那地尔处理的4组,丙二醛则不同程度的低于对照组,结论：吡那地尔诱导心脏超极化停跳以及药物预处理,有助于降低心肌ATP的消耗,减少脂质过氧化物的形成,明显改善离体兔心脏缺血／再灌注后期心功能。     

31P-NMR study of cardiac preservation: St. Thomas' Hospital cardioplegic solution versus UW preservation solution

Abstract. Ex vivo cardiac preservation was evaluated by measuring the catabolism of high-energy phosphate (ATP and creatine phosphate, CrP) using ³¹P-NMR spectroscopy. After cardioplegic arrest St. Thomas' Hospital cardioplegic solution (group A), and University of Wisconsin (UW) preservation solution (group B) were tested. The hearts were mounted in the 4.7 T horizontal bore magnet of the NMR spectrometer and were continuously perfused with the test solution under 25 cm H₂O pressure for 6 h at 10°C. Peak heights of the β-phosphate of ATP and CrP were measured and expressed as percentages of the initial value. For both group A and group B, ATP declined less rapidly during preservation than CrP. In group A, ATP remained constant for 60 min while CrP decreased from the onset of preservation. After 6 h of preservation 28.3% of ATP and 24.5% of CrP remained (group A). On the other hand, in group B, levels of both ATP and CrP remained much more stable: CrP did not decrease during the first 3 h of preservation, while ATP started to decrease after 5 h. At the end of preservation 76.1% of ATP and 71.5% of CrP were still present. We conclude that UW solution is superior to St. Thomas' Hospital solution for the preservation of high-energy phosphates during 6 h cardiac preservation with continuous hypothermic low-flow perfusion.     

31P-NMR study of cardiac preservation: St. Thomas' Hospital cardioplegic solution versus UW preservation solution

Ex vivo cardiac preservation was evaluated by measuring the catabolism of high-energy phosphate (ATP and creatine phosphate, CrP) using ³¹P-NMR spectroscopy. After cardioplegic arrest St. Thomas' Hospital cardioplegic solution (group A), and University of Wisconsin (UW) preservation solution (group B) were tested. The hearts were mounted in the 4.7 T horizontal bore magnet of the NMR spectrometer and were continuously perfused with the test solution under 25 cm H₂O pressure for 6 h at 10°C. Peak heights of the -phosphate of ATP and CrP were measured and expressed as percentages of the initial value. For both group A and group B, ATP declined less rapidly during preservation than CrP. In group A, ATP remained constant for 60 min while CrP decreased from the onset of preservation. After 6h of preservation 28.3% of ATP and 24.5% of CrP remained (group A). On the other hand, in group B, levels of both ATP and CrP remained much more stable: CrP did not decrease during the first 3 h of preservation, while ATP started to decrease after 5 h. At the end of preservation 76.1% of ATP and 71.5% of CrP were still present. We conclude that UW solution is superior to St. Thomas' Hospital solution for the preservation of high-energy phosphates during 6 h cardiac preservation with continuous hypothermic low-flow perfusion.     

St. Thomas' Hospital cardioplegic solution. Beneficial effect of glucose and multidose reinfusions of cardioplegic solution

The intention of this study was to determine whether glucose is beneficial in a cardioplegic solution when the end products of metabolism produced during the ischemic period are intermittently removed. The experimental model used was the isolated working rat heart, with a 3-hour hypothermic 10 degrees C cardioplegic arrest period. Cardioplegic solutions tested were the St. Thomas' Hospital No. 2 and a modified Krebs-Henseleit cardioplegic solution. Glucose (11 mmol/L) was beneficial when multidose cardioplegia was administered every 30 minutes. Including glucose in Krebs-Henseleit cardioplegic solution improved postischemic recovery of aortic output from 57.0% +/- 1.8% to 65.8% +/- 2.2%; p less than 0.025. The addition of glucose to St. Thomas' Hospital No. 2 cardioplegic solution improved aortic output from 74.6% +/- 1.9% to 87.4% +/- 1.9%; p less than 0.005. Furthermore, a dose-response curve showed that a glucose concentration of 20 mmol/L gave no better recovery than 0 mmol/L, and glucose in St. Thomas Hospital No. 2 cardioplegic solution was beneficial only in the range of 7 to 11 mmol/L. In addition, we showed that multidose cardioplegia was beneficial independent of glucose. Multidose St. Thomas' Hospital No. 2 cardioplegia, as opposed to single-dose cardioplegia, improved aortic output recovery from 57.4% +/- 5.2% to 74.6% +/- 1.9%; p less than 0.025, and with St. Thomas' Hospital No. 2 cardioplegic solution plus glucose (11 mmol/L) aortic output recovery improved from 65.9% +/- 2.9% to 87.4% +/- 1.9%; p less than 0.005. Hence, at least in this screening model, the St. Thomas' Hospital cardioplegic solution should contain glucose in the range of 7 mmol/L to 11 mmol/L, provided multidose cardioplegia is given. We cautiously suggest extrapolation to the human heart, on the basis of supporting clinical arguments that appear general enough to apply to both rat and human metabolisms.     

牛血红蛋白用于兔离体心脏延时保存的研究

目的 研究牛血红蛋白对兔离体心脏保存时限的作用。方法 在Ｓｔ Ｔｈｏｍａｓ Ⅱ液中加入无机质游离牛血红蛋白（ＳＦＢＨＢ）,用该液常温灌注离体兔心６ｈ作为实验组,用单纯Ｓｔ ＴｈｏｍａｓⅠ液低温保存离体兔心作为对照组,每组大白兔均为１２只。结果 左室发展压（ＬＶＤＰ）,冠状动脉流量恢复率（ＣＲＦ）,实验组均显著高于对照组,Ｐ〈０．００;１兔心保存４ｈ后,心肌组织ＡＴＰ含量两组差异显著;心脏复跳３０ｍ     

Long-term myocardial preservation: beneficial and additive effects of polarized arrest (Na+-channel blockade), Na+/H+-exchange inhibition, and Na+/K+/2Cl- -cotransport inhibition combined with calcium desensitization

BACKGROUND: Polarized arrest, induced by tetrodotoxin (TTX) at an optimal concentration of 22 micromol/L, has been shown to reduce ionic imbalance and improve myocardial preservation compared with hyperkalemic (depolarized) arrest. Additional pharmacologic manipulation of ionic changes (involving inhibition of Na+ influx by the Na+/H+ exchanger [HOE694] and Na+/K+/2Cl- cotransporter [furosemide], and calcium desensitization [BDM]) may further improve long-term preservation. In this study, we (i) established optimal concentrations of each drug, (ii) determined additive effects of optimal concentrations of each drug and (iii) compared our optimal preservation solution to an established depolarizing cardioplegia (St Thomas' Hospital solution No 2: STH2) used during long-term hypothermic storage for clinical transplantation. METHODS: The isolated working rat heart, perfused with Krebs Henseleit (KH) buffer was used; cardiac function was measured after 20 min aerobic working mode perfusion. The hearts (n=6/group) were arrested with a 2 ml infusion (for 30 sec) of the polarizing (control) solution (22 micromol/L TTX in KH) or control+drug and subjected to 5 hr or 8 hr of storage at 7.5 degrees C in the arresting solution. Postischemic function during reperfusion was measured (expressed as percentage of preischemic function). RESULTS: Dose-response studies established optimal concentrations of HOE694 (10 micromol/L), furosemide (1.0 micromol/L) and BDM (30 mmol/L) in the polarizing (control) solution. Sequential addition to the control solution (Group I) of optimal concentrations of HOE694 (Group II), furosemide (Group III), and BDM (Group IV) were compared with STH2 (Group V); postischemic recovery of aortic flow was 29+/-7%, 49+/-6%*, 56+/-2%*, 76+/-3%*, and 25+/-6%, respectively (*P<0.05 vs. I and V). Creatine kinase leakage was lowest, and myocardial ATP content was highest in Group IV. CONCLUSIONS: A polarizing preservation solution (KH+TTX) containing HOE694, furosemide, and BDM significantly enhanced long-term preservation compared with an optimized depolarizing solution (STH2) used clinically for long-term donor heart preservation.     

U50488H联合东莨菪碱对大鼠离体心脏的保护作用

目的 探讨k阿片受体激动剂U50488H联合东莨菪碱对大鼠离体心脏低温保存的保护效果其作用机制.方法 54只SD大鼠随机分为9组,每组6只,用U50488H、东莨菪碱及KATP阻断剂(5-HD)组合后进行心脏保存.采用LangendorffⅢ心脏灌注和工作模型装置进行心脏功能测定,比较低温保存6h后心功能恢复率、心肌含水量、能量变化,观察心肌超微结构改变.结果 U50488H+东莨菪碱组左心室功能和结构损伤最轻,单用U50488H、东茛菪碱、St.Thomas液组左心室功能和结构损伤较轻,而对照组左心室功能和结构损伤严重;U50488H+东莨菪碱组心功能恢复率最快、细胞ATP含量最高,其次是单用U50488tt、东莨菪碱、St.Thomas液组.加用5-HD时,U50488tt+东莨菪碱组合各项指标变化不显著,但单用U50488H、东莨菪碱组各项指标变化显著,差异也有统计学意义(P＜0.05).结论 U50488H、东莨菪碱对大鼠离体心脏在6 h内有明显的保护作用,达到St.Thomas液水平,两者联合使用时效果更佳.开放mitoKATP,通道可能是发挥保护作用的重要机制.     

Mechanisms of myocardial protection by adenosine-supplemented cardioplegic solution: myofilament and metabolic responses

OBJECTIVE: Adenosine supplementation of cardioplegic solutions in cardiac operations improves postarrest myocardial recovery after cardioplegic arrest and reperfusion; however, the mechanism of the action of adenosine remains unknown. We tested the hypotheses that adenosine-supplemented cardioplegic solution improves myofibrillar protein cooperative interaction and increases myocardial anaerobic glycolysis. METHODS: The hearts of male Sprague-Dawley rats were randomized to undergo 120 minutes of cardioplegic arrest with 1 of 3 cardioplegic solutions: (1) St Thomas' Hospital No. 2 cardioplegic solution (St Thomas group), (2) St Thomas' Hospital No. 2 cardioplegic solution plus adenosine (100 micromol/L) (adenosine group), and (3) St Thomas' Hospital No. 2 cardioplegic solution plus adenosine (100 micromol/L) plus the nonspecific adenosine receptor antagonist 8-p -sulfophenyltheophylline (50 micromol/L) (sulfophenyltheophylline group). A fourth group of hearts underwent no cardioplegic arrest. RESULTS: Systolic and diastolic functional recovery was improved in the adenosine group compared with that in the other two groups, independent of coronary flow. Adenosine supplementation of cardioplegic solution prevented the decrease in myofibrillar protein cooperative interaction seen after cardioplegic arrest and reperfusion (St Thomas and sulfophenyltheophylline groups). Adenosine-supplemented cardioplegic solution also caused significantly increased anaerobic glycolysis during cardioplegic arrest. These responses were blocked in the sulfophenyltheophylline group. CONCLUSIONS: The changes in myocardial glycolytic activity and myofilament cooperativity coincided with functional recovery in the three cardioplegia groups and may represent mechanisms underlying protection with adenosine-supplemented cardioplegic solution.     

U50 488H预处理及低温保存对离体兔心的保护作用

目的观察U50 488H预处理及低温保存对离体兔心的保护作用。方法将40只大白兔均分为5组，每组8只。通过Langendorff装置建立离体心脏灌注模型，对照组：不用药物进行预处理，用UW液保存心脏6h；组Ⅰ：用含U50 488H（1．6mmol／L）的St．ThomasⅡ心脏停搏液预处理，离体心脏低温保存4h；组Ⅱ：预处理同组Ⅰ，低温保存6h；组Ⅲ：预处理同组Ⅰ，低温保存8h；组Ⅳ：预处理同组Ⅰ，低温保存10h。离体心脏在再灌注30min后检测心功能、心肌肌浆网钙离子三磷酸腺苷酶（SRCa^2＋-ATPase）活性和心肌线粒体Ca^2＋浓度。结果随着离体心脏低温保存时间的延长，心功能各项指标的恢复率、冠状动脉流量（Cf）的恢复率和SRCa^2＋-ATPase的活性呈下降趋势，而线粒体Ca^2＋浓度随着心脏低温保存时间的延长而逐渐升高。组Ⅰ和组Ⅱ上述心功能指标恢复率分别高于组Ⅲ和组Ⅳ（P〈0．05，0．01），组Ⅲ恢复率高于组Ⅳ（P〈0．05）。组ⅡCf的恢复率（84．56％±10．38％）高于组Ⅲ（79．45％±9．67％）、组Ⅳ（68．31％±6．84％，P〈0．01），组Ⅲ高于组Ⅳ（P〈0．05）。组ⅡSRCa^2＋-ATPase的活性（4．43±0．41μmol／mg·h）分别高于对照组（3．04±0．22μmol／mg·h）、组Ⅲ（3．26±0．29μmol／mg·h）和组Ⅳ（2．57±0．63μmol／mg·h，P〈0．05），组Ⅲ高于组Ⅳ（P〈0．01）。组Ⅱ线粒体Ca^2＋浓度（38．76±4．30μmol／g·dw）和对照组（40．23±3．75μmol／g·dw）分别低于组Ⅲ（43．25±5．16μmol／g·dw）和组Ⅳ（45．78±3．26μmol／g·dw，P〈0．05，0．01）。结论U50 488H预处理及U50 488H保存液对离体供心的低温保存时间应控制在8h以内；UW液对离体心脏的保存作用与U50 488H预处理及低温保存6h效果相当。