心脏直视手术再灌注心肌组织自由基及超微结构改变

作者对１５例心脏直视手术患者心肌组织丙二醛（ＭＤＡ）含量及超氧化物岐化酶（ＳＯＤ）活性进行测定，并对心肌组织进行超微结构改变观察。结果表明，心肌组织ＭＤＡ含量在缺血再灌注后明显增加而ＳＯＤ活性明显下降。心脏复跳后心肌组织超微结构损害较心脏停跳后更明显。提示心肌组织氧自由基的产生主要是在再灌注期，是心肌组织缺血再灌注损伤的重要原因。     

Oxygen free radical generation in ischemic-reperfused myocardium of rat in vivo

Many studies have provided indirect evidence that there is a relationship between oxygen free radical and myocardial ischemic-reperfusion injury. In this study, we applied ESR spectroscopy to measure oxygen free radical generation in the acutely ischemic-reperfused heart of rat in vivo. The experimental model was established by 45 min ligation of the left anterior descending coronary artery (LAD) and 10 min reperfusion in vivo. The myocardial samples taken for ESR measurement were fresh-freezing tissue pieces. Meanwhile, the tissue ultrastructure was observed. We also observed the protective effect of superoxide dismutase (SOD) on myocardial ischemic-reperfusion injury. The results showed: 1. Large amounts of oxygen free radical were generated in the course of postischemic reperfusion. The amount of oxygen free radical produced in this process was positively related to the extent of myocardial damage. Oxygen free radical was at least one of the major cause of rat myocardial reperfusion injury observed in this experiment. 2. SOD could scavenge oxygen free radical and prevent or reduce reperfusion injury of rat heart in vivo.     

缺血预适应对未成熟大鼠心肌线粒体及能量代谢的影响

目的研究内源性心肌保护机制一缺血预适应（Ｉｓｃｈｅｍｉｃ－ｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇ,ＩＰＣ）对未成熟心肌线粒体及能量代谢的 影响,并探讨其作用机制。方法采用改良Ｌａｎｇｅｎｄｏｒｆｆ－Ｎｅｅｌｙ离体鼠心灌流装置,建立未成年大鼠（４周龄）离体心脏顺 行灌注左心作功模型。３６只大鼠随机等分为缺血对照组（ＮＣ）、Ｓｔ．ＴｈｏｍａｓⅡ晶体停搏液组（ＳＴ）、预缺血加停搏液组 （ＰＩ）。比较再灌注后各组心功能（ＬＷＳＰ,ＬＶＥＤＰ,±ｄｐ／ｄｔｍａｘ,ＣＯ）的恢复率;测定缺血前、再灌注后线粒体游离钙（Ｃａ２＋）、 丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）及心肌ＡＴＰ含量;观察再灌注后心肌及线粒体超微结构的变化。结果 ＩＰ组心 功能指标的恢复率明显好于ＳＴ组和ＮＣ组（Ｐ＜０．０５）;再灌注后ＳＴ组、ＮＣ组心肌线粒体Ｃａ２＋、ＭＤＡ含量明显增高, ＳＯＤ含量明显减少（Ｐ＜０．０５）,而 ＩＰ组则无明显变化;ＩＰ组、ＳＴ组 ＡＴＰ含量无显著差别,均明显高于 ＮＣ组;ＳＴ组、ＮＣ 组心肌及线粒体超微结构破坏明显,ＩＰ组则仅有轻微改变。结论Ｓｔ．ＴｈｏｍａｓⅡ晶体停搏液能减轻未成熟心肌能量损耗, 但对心肌线粒体的保护作用较小,影响了     

萘甲异喹对大鼠心肌缺血再灌注损伤的保护作用

目的：观察萘甲异喹（NI）对氧自由基损伤心肌的影响。方法：采用大鼠离体互作心脏，观察NI对心肌缺血再灌注损伤的保护作用。结果：NI显著保护心肌超氧化物歧化酶（SOD）活力的降低；减少心肌丙二醛（MDA）生成；减少心肌肌酸磷酸激酶（CPK）释放；降低心肌细胞内钙聚集；降低再灌注诱发的室颤（VF）和室速（VT）发生率；并减轻心肌超微结构的损伤。结论：NT对缺血再灌注损伤心肌的保护与其抗氧自由基作用有关。     

心肌缺血再灌注损伤中纳洛酮的抗氧化作用

目的 在大鼠离体心脏缺血再灌注模型上,观察纳洛酮对大鼠心肌氧自由基代谢的影响,探讨纳洛酮对心脏作用的可能机制.方法 建立改良的Langendofff离体大鼠心脏灌注模型,缺血40min,再恢复常速灌注30min,造成心肌缺血再灌注损伤.利用该模型观察给予不同浓度的纳洛酮后大鼠心肌SOD活性及MDA含量的变化.结果 模型组与对照组比较,心肌MDA含量增加,SOD活力降低;给予两种不同浓度的纳洛酮分别灌注缺血的心脏后,与对照组比较,纳洛酮16mg/L和32mg/L可减少心肌MDA生成量,并提高SOD活力.结论 纳洛酮对大鼠再灌注损伤心脏的具有保护作用,其机制与抗氧化作用有关.     

七氟醚和异氟醚对心脏换瓣术患者术中氧自由基代谢的影响

将３０例心脏瓣膜置换术患者随机分为七氟醚组、异氟醚组及对照组，观察七氟醚和异氟醚对心肌缺血／再灌注过程中血浆过氧化脂质（ＬＰＯ）含量、红细胞超氧化物歧化酶（ＳＯＤ）活性的影响，探讨吸入麻醉药的心肌保护作用。结果显示：术中三组病人红细胞ＳＯＤ活性无明显变化，两吸入药组血浆ＬＰＯ含量无明显上升（Ｐ＞０．０５）；两吸入药组开主动脉后心脏自动复跳率均高于对照组，异氟醚组尤甚。提示七氟醚与异氟醚能抑制心脏换瓣术患者心肌缺血／再灌注过程中血浆ＬＰＯ水平的上升，能减轻自由基介导的心肌缺血／再灌注损伤。     

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。     

Alterations of mitochondrial function in ischemia/reperfusion cat heart

The effect of myocardium being subjected to 60 min ischemia and 60 min reperfusion incat cardiopulmonary bypass on level of lipid peroxides(LPO),function of myocardial mitochon-dria and activity of superoxides dismutase(SOD)was studied. Myocardial mitochondrial functionwas depressed slightly 60 rain after ischemia but significantly 60 min after reperfusion.Increasedlipid peroxides content and decreased activity of SOD were observed at 60 rain after ischemia.Af-ter reperfusion,the activity of SOD continued decreasing,and LPO elevated still further.Theseresults support the hypothesis that free radicals may contribute to myocardial reperfusion injury.