急性心肌梗死家兔心肌MtATPase表达和心肌细胞凋亡的变化

目的： 研究急性心肌梗死后线粒体能量代谢和心肌细胞凋亡的动态变化,探讨二者在缺血心肌细胞演变中的作用和意义。方法: 结扎家兔左冠状动脉主干建立实验性心肌梗死（AMI）模型,采用酶组织化学染色法和脱氧核苷转移酶介导的缺口末端标记技术检测梗死后0.5、1、2、4、8、12 h左室前壁线粒体腺苷三磷酸酶（MtATPase）和细胞凋亡的变化,结合显微图像分析技术定量测定酶活性平均积分吸光度值（IA）和凋亡指数（AI）。结果: (1)AMI 2 h,MtATPase表达开始下降,4 h显著减低,随着缺血时间延长,表达持续下降, 2、4、8、12 h IA分别为168.09±3.75、159.01±2.62、143.12±3.47和127.65±4.64,与对照组比较有明显差异（P<0.05）;(2)AMI 0.5 h仅见少数凋亡心肌细胞,随缺血时间延长,凋亡细胞数目显著增加,4 h达到高峰,然后开始下降,但12 h仍高于对照组, 0.5、1、2、4、8、12 h AI分别为4.74±0.75、10.96±1.06、17.28±1.75、26.83±2.06、20.41±1.52和8.91±0.74,与对照组比差异显著（P<0.01）。结论: 细胞凋亡是AMI心肌细胞一种重要的死亡形式,梗死心肌细胞的演变和线粒体能量代谢密切相关。     

参麦注射液对大鼠心肌缺血再灌注损伤的保护效应及其与热休克蛋白的关系

目的 :研究参麦注射液对大鼠心肌缺血再灌注损伤的保护效应以及与热休克蛋白 (HSP70 )的关系。方法 :用在体左冠状动脉前降支穿线结扎法制备心肌缺血再灌注模型。 60只SD大鼠分为三组 ,假手术组n =10只 ,缺血再灌注组n =2 5只 ,参麦注射液干预组n =2 5只。缺血 3 0min ,再灌注 12 0min。观察心肌梗死范围和心肌细胞超微结构变化 ,采用S P免疫组化法 ,检测HSP70 的表达。结果 :参麦注射液干预组与缺血再灌注组相比 ,缺血面积 ( % ) ( 3 8.3 6± 2 .62vs 42 .3 2±2 .2 8,P <0 .0 1) ;梗死面积 ( % ) ( 59.3 6± 2 .44vs 65.63± 1.68,P <0 .0 1)。HSP70 表达 ( 0 .13 8± 0 .0 2 2vs 0 .12 2± 0 .0 18,P <0 .0 1)。电镜下 ,缺血再灌注组 ,肌纤维挛缩 ,核固缩 ,线粒体嵴疏松 ,空泡形成。参麦注射液干预后 ,肌节清晰 ,线粒体嵴较密集 ,无明显空泡形成。结论 :参麦注射液能保护心肌超微结构 ,缩小缺血、梗死范围 ,其机制可能与HSP70 的表达增加有关     

钙敏感受体在大鼠心肌缺血/再灌注损伤的表达变化及与心肌损伤关系

目的： 观察钙敏感受体（CaSR）在大鼠心肌缺血/再灌注时的表达变化，揭示其与心肌缺血/再灌注损伤的关系。方法： Wistar大鼠随机分为5组：假手术组（sham组）、缺血再灌注1、2、4和6 h组（I/R 1 h、2 h、4 h、6 h组）。采用冠状动脉结扎和松结的方法，复制大鼠在体心肌缺血/再灌注损伤模型，记录左室收缩压（LVSP）和左室内压最大变化速率（±dp/dtmax），测定血清LDH、SOD活性和MDA含量，透射电镜观察心肌超微结构变化， RT-PCR法检测心肌组织中CaSR mRNA的表达变化。结果：LVSP、左室内压±dp/dtmax及SOD活性随再灌注时间延长而减低，LDH活性和MDA含量在再灌注2 h时最高；心肌超微结构损伤在再灌注1 h、2 h较重，随再灌注时间延长而减轻；大鼠心肌缺血/再灌注1 h、2 h心肌组织CaSR的mRNA表达升高，再灌注4 h、6 h后降低。结论： CaSR mRNA表达多时心肌损伤较重，CaSR可能参与了心肌缺血/再灌注损伤。     

脑缺血大鼠大脑皮质NMDA受体的早期表达

目的　探讨脑缺血和缺血再灌注早期大脑皮质NMDA受体的变化规律。方法　健康雄性SD大鼠 4 8只 ,随机分为 6组 :假手术对照组、单纯脑缺血 1 5min、2 0min和 30min组及脑缺血 1 5min再灌流 30min和 2 4h组 ;4血管脑缺血动物模型 ;连续冰冻冠状切片观察 ,NR1 免疫组化染色特异性地显著NMDA受体的变化 ,图象分析及计算阳性单位PU值。结果　①单纯脑缺血各组PU值分别为 7 5 5± 1 81、6 91± 2 5 3和 6 0 9± 1 5 0 ,与对照组PU值 9 0 4± 1 5 7相比呈下降趋势 (P≤ 0 0 5 ) ;②再灌流 30min和 2 4h组PU值分别为 5 76± 2 2 4和 4 73± 1 34,与对照组PU值相比明显减少 36 2 9%～ 4 7 6 8% ,有统计学意义(P <0 0 5 ) ;③再灌流 0min、30min和 2 4h组两两比较 ,除 2 4h和 0min组相比NR1 阳性反应物减少有统计学意义 (P <0 0 5 )外 ,其它组别间NMDA受体下降的变化无显著性差异 (P >0 0 5 )。结论　脑缺血和缺血再灌流早期NMDA受体都存在下行调节 ,这种调节可能是一种保护性作用     

树鼩血栓性脑缺血时单胺氧化酶活性的变化及银杏内酯B作用机制探讨

目的 :揭示血栓性脑缺血时缺血区和血清单胺氧化酶 (MAO)活性变化及对血小板活化因子 (PAF)受体拮抗剂银杏内酯B(GB)作用机理的探讨。方法 :建立光化学诱导树鼠句血栓性脑缺血模型 ,用酶比色法测量缺血后4、2 4及 72h中心区、半暗区、对侧区及血清的MAO活性 ,并用双缩脲法测定上述各区的蛋白含量。结果 :脑缺血后不同时间缺血中心区MAO活性显著低于假手术组 [(15 4 1± 1 6 3)× 10 3 U/g蛋白 ]或对侧区 [(15 4 7± 1 6 8)× 10 3 U/g蛋白 ],以 72h最为明显 [(2 19± 1 96 )× 10 3 U/g蛋白 ,P <0 0 1];此时缺血半暗区和血清MAO活性 [分别为 (2 5 30± 2 0 1)× 10 3 U/g蛋白和 (2 10 0 4± 2 6 6 7)× 10 3 U/L]明显高于假手术组 (P <0 0 1)。光化学反应后 6h舌下静脉一次注射PAF受体拮抗剂GB(5mg·kg-1)后 2 4h时 ,半暗区MAO活性明显低于缺血组 ,而中心区则高于缺血组 (P <0 0 1)。MAO活性变化与相应区域蛋白含量改变一致 (r=0 81,P <0 0 5 )。结论 :脑缺血后中心区、半暗区MAO活性改变是相应区域单胺类递质消长变化的主要原因 ,MAO活性变化与神经元蛋白质合成能力的改变有关 ;GB的脑保护作用与其拮抗PAF受体和调节MAO活性而促进递质平衡有关。     

哮喘豚鼠MMP-9、TIMP-1免疫反应的变化及与气道重塑的关系

目的　观察实验性哮喘豚鼠气道平滑肌基质金属蛋白酶 9(MMP 9)及其抑制剂 (TIMP 1)的表达以及气道平滑肌厚度的变化。方法　用免疫组织化学结合显微图像分析测定气道平滑肌MMP 9、TIMP 1免疫反应的变化及气道平滑肌厚度。结果　MMP 9、TIMP 1广泛分布于气道平滑肌。哮喘组MMP 9平均灰度值(10 5 94± 6 0 9)明显低于对照组 (12 0 2 5± 3 6 6 ) (P <0 0 1) ;哮喘组TIMP 1平均灰度值 (99 36± 5 71)明显低于对照组 (12 3 4 5 7) (P <0 0 1) ;哮喘组气道平滑肌厚度 (6 45± 1 83μm2 / μm)明显高于对照组 (3 17± 0 85 )(P <0 0 5 )。结论　MMP 9、TIMP 1可能参与哮喘时气道重塑。     

粉防己碱预处理对心肌缺血/再灌注损伤大鼠肿瘤坏死因子-α表达及核因子-κB活化的影响

目的 探讨粉防己碱预处理对心肌缺血/再灌注过程中大鼠肿瘤坏死因子-α表达及与核因子-кB活化的影响以及相关关系.方法 60只SD大鼠随机分为3组缺血/再灌注损伤组、假手术组、粉防己碱治疗组,缺血/再灌注损伤组结扎大鼠左前降支造成心肌缺血30 min后再灌注24 h后处死大鼠;假手术组只穿针不结扎,余步骤同缺血/再灌注损伤组;粉防己碱治疗组在缺血前30 min腹腔注射粉防己碱,余步骤同缺血/再灌注损伤组.24 h后取心肌标本,用酶联免疫吸附法检测心肌组织中肿瘤坏死因子-α表达水平,凝胶电泳迁移率变化分析检测核因子-κB的活性.结果 粉防己碱组与缺血再灌注组相比肿瘤坏死因子-α表达水平明显减低(208.40±25.12 VS 306.65±17.78,P＜0.01)而与假手术组相比表达明显增强(208.40±25.12 VS 61.45±9.20,P＜0.01).粉防己碱组核因子-κB的活性明显低于缺血再灌注组(29.58±1.56 VS 40.33±4.39,P＜0.01)而与假手术组无显著性差异(29.58±1.56 VS 30.09±3.46,P＞0.05).结论 粉防己碱预处理可以使心肌缺血/再灌注损伤过程中肿瘤坏死因子-α生成明显减少,核因子-кB的活化受到有效抑制,从而起到减轻心肌缺血/再灌注损伤的作用.     

急性心肌梗死大鼠血清血管内皮生长因子含量的变化

目的和方法 :探讨急性心肌梗死大鼠模型血清血管内皮生长因子 (VEGF)含量的变化及其意义。 88只雄性SD大鼠 ,其中 80只结扎左冠状动脉导致心肌梗死 ,8只开胸但不结扎冠状动脉作对照组。于心肌梗死后 1h ,3h ,6h ,12h ,2 4h和 2d ,3d ,5d ,7d ,14d分别从右心房抽取血样品 (n =8)。用敏感、特异的酶连接免疫吸附测定法测定血清样品中的VEGF含量。结果 :8只假手术对照鼠的血清VEGF浓度为 (6 6 99± 17 83)pg/mL。心肌梗死后 6h组血清VEGF水平达到 (12 5 6 8± 2 8 0 7)pg/mL(与对照组比P <0 0 1) ,结扎后 2 4h组达高峰 (2 40 6 1± 70 6 3pg/mL ,与对照组比P <0 0 1) ,然后逐渐下降 ,但术后 14d组仍显著高于对照组 (10 7 6 4±30 13pg/mL ,P <0 0 1)。结论 :心肌梗死大鼠血清VEGF水平持续显著升高 ,可能对心肌梗死后的血管生成起重要作用     

大鼠心肌缺血/再灌注损伤模型的改进与评价

大鼠心肌缺血 /再灌注损伤是模拟人类心梗及溶栓再通治疗 ,研究缺血预适应机制 ,评价抗心律失常药物疗效常用的动物模型。本文在传统造模方法的基础上进行了一定的改进 ,采用在压管下加一小垫片的方法 ,减少了传统推管法对心表面的机械损伤 ,方法简便 ,冠脉阻断确实。结果 :大鼠左冠状动脉主干缺血30′,再灌 12 0′,危险区 /左室重量比为 5 5 %± 5 % ,坏死区 /危险区为 5 8%± 6 % (N =10 )。心肌酶谱结果 :CK430 1± 2 5 1u/l,CK- MB 2 2 88± 32 8u/l,L DH 2 32 9± 2 16 u/l,AST 371± 5 7u/l(N=5 )。     

一氧化氮在实验性缺血再灌注心肌顿抑中的作用及左旋精氨酸干预

目的 :为了探讨一氧化氮 (ＮＯ)在实验性缺血再灌注心肌顿抑中的作用及左旋精氨酸 (Ｌ -Ａｒｇ)对其的影响。方法 :选用 2 0只家兔 ,制备心肌缺血再灌注模型 ,随机均分为对照组和Ｌ -Ａｒｇ组 ,分别于缺血前、缺血 40ｍｉｎ及再灌注 2 0ｍｉｎ取血检测ＮＯ水平 ,相应时点监测心功能。结果 :心肌缺血再灌注期间 ,一氧化氮代谢产物含量 (ＮＯＰ)显著下降 (缺血前 2 6 9± 4 6μｍｏｌ/Ｌ ,缺血 40ｍｉｎ 1 4 8± 3 8μｍｏｌ/Ｌ ,再灌注 2 0ｍｉｎ 1 2 7± 5 3μｍｏｌ/Ｌ ,Ｐ均 <0 0 0 1 ) ;心肌舒缩功能指标 (ＭＡＰ、ＬＶＳＰ、 ｄｐ/ｄ…     

CGRP和NGF对全脑缺血再灌注大鼠脑组织PKC表达的调节作用

目的　研究大鼠脑缺血再灌注后蛋白激酶C(proteinkinaseC ,PKC)在海马和顶叶皮质的表达 ,探讨降钙素基因相关肽 (CGRP)和神经生长因子 (NGF)对脑组织缺血再灌注的保护作用及机制。方法　采用颈动脉负压分流法制作大鼠脑缺血再灌注模型 ,采用免疫组织化学SABC法及显微图像分析检测海马及皮质内PKC的表达。结果　大鼠缺血再灌注海马CA1区及顶叶皮质内PKC阳性产物平均灰度值较正常组低 (P <0 .0 5 ) ,注射CGRP或NGF后PKC阳性产物平均灰度值明显高于缺血再灌注组 (P <0 .0 1) ,二者联合应用时平均灰度值比单独应用高 (P <0 .0 1)。结论　CGRP及NGF参与缺血神经元PKC的调节 ,二者对缺血神经元有协同保护作用     

Ischemic postconditioning and size of myocardial infarction during inhibition of norepinephrine reuptake

We studied the effect of inhibition of norepinephrine reuptake during the reperfusion period on the size of infarction zone after focal myocardial ischemia and under conditions of ischemic postconditioning. In groups 1 and 2, 30-min occlusion of the left coronary artery followed by 120-min reperfusion was performed. In groups 3 and 4, ischemia was followed by ischemic postconditioning (six 10-sec occlusions alternating with 10-sec reperfusions). Ringer solution (1 ml, groups 1 and 3) and desipramine (0.8 mg/kg, groups 2 and 4) were injected intravenously at the beginning of reperfusion. The area of myocardial infarction in group 1 was 32.0 ± 3.1% of the area of the risk zone; in groups 2, 3, and 4 the corresponding value was 46.1 ± 3.4% (p = 0.006), 22.2 ± 2.6% (p = 0.028), and 50.3 ± 3.1% (p = 0.018), respectively. It was shown that inhibition of norepinephrine reuptake in the early reperfusion period after ischemia increased myocardial injury and abolished the protective effect of ischemic postconditioning.     

慢性脑缺血对青年和老年大鼠海马NOS阳性神经元的影响

本文利用组织化学方法观察了慢性脑缺血对青、老年大鼠海马ＮＯＳ阳性神经元的影响。慢性脑缺血采用双侧颈总动脉永久性结扎模型。结果：青年缺血１ 月组大鼠海马ＣＡ１、ＣＡ２～３ 和ＤＧ 亚区ＮＯＳ阳性神经元面数密度分别为２９．１±２．３、２３．５±２．１ 和３９．３±２．８,小于对照组相应三个亚区（４９．６±１．３、４９．３±２．１ 和６４．７±２．１）,Ｐ＜ ０．０１;青年缺血３ 月组大鼠ＣＡ１、ＣＡ２～３ 和ＤＧ 亚区ＮＯＳ阳性神经元面数密度分别为４０．２±１．６、３９．３±２．５ 和４８．４±１．８,和对照组者相近,但大于缺血１ 月组（Ｐ＜ ０．０１）。老年缺血１ 月组大鼠海马各区ＮＯＳ阳性神经元面数密度分别为３９．６±１．５、３５．６±２．１ 和５４．７±２．５,小于老年对照组相应三个亚区（５５．８±１．７、５１．３±１．７ 和６４．９±１．９）,Ｐ＜ ０．０１;老年缺血３ 月组大鼠各亚区ＮＯＳ阳性神经元面数密度分别为４３．１±２．４、３８．７±３．４ 和５４．７±３．２,仍然小于对照组,Ｐ＜ ０．０１。结果提示：慢性脑缺血可以影响大鼠海马ＮＯＳ阳性神经元,但青年和老年大鼠海马ＮＯＳ神经元对慢性脑缺血损伤的易感性和反应性不同。     

缺血后适应减轻树鼩缺血性脑水肿及脑梗死的机制

目的 观察缺血后适应对树鼩血栓性脑缺血时大脑皮层脑水含量、局部脑血流、梗塞面积及神经元超微结构的影响,探讨其对树鼩脑缺血时神经保护的可能机制。 方法 将88只健康成年树鼩随机分为对照组、脑缺血4 h组、脑缺血24 h组、后适应4 h组及后适应24 h组（每组n=8）,另取8只动物做HE染色（n=3）及电子显微镜观察（n=5）。本实验采用光化学反应诱导树鼩血栓性脑缺血而建立脑缺血动物模型,在脑缺血模型建成后4 h夹闭缺血侧颈总动脉5 min,再灌注5 min,如此交替进行3个循环以建立缺血后适应模型。测定大脑皮层局部脑血流,脑组织含水量,脑梗死范围,并观察皮层及海马CA1区神经元超微结构改变。 结果 脑缺血时神经元固缩,线粒体肿胀,嵴溶解或形成空泡,内质网肿胀,内质网池形成。缺血后适应能使海马CA1区神经元固缩减少,线粒体和内质网的病理改变减轻,细胞水肿改善。随着缺血时间的延长,缺血24h组脑水含量明显增加86.81%±1.08%,此时脑梗塞面积明显扩大33.00%±3.03%,局部脑血流明显降低（134.27±28.75）ml/min。缺血后适应24h组脑组织含水量明显减少（81.04%±1.04%,P＜0.01）;脑梗塞面积缩小（16.79%±1.29%,P＜0.01）;而局部脑血流明显增加［（195.25±21.18）ml/min,P＜0.01］。 结论 缺血后适应可缓解树鼩缺血性脑水肿并缩小梗死范围,其机制可能与改善局部脑血流有关。     

Stem cell implantation in the treatment of peripheral vascular disease

Treatment options of ischemic vascular disease of the lower limbs are a challenged field that necessitates new therapeutic modalities. Stem cell transplantation offers a promising achievement of therapeutic angiogenesis in patients with ischemic limbs. Our study investigated the efficacy and safety of the implantation of autologous peripheral blood mononuclear cells (PBMNCs) mobilized by granulocyte colony-stimulating factor (G-CSF) in patients with chronic limb ischemia. Twenty-four patients with chronic lower limb ischemia were enrolled and divided randomly into two groups: the implanted group (n?=?12) and the control group (n?=?12). In the implanted group, the patients received subcutaneous injections of recombinant human G-CSF (300 μg/day) for 5 days to mobilize stem/progenitor cells, and their PBMNCs were harvested using a blood cell separator and were implanted by multiple intramuscular injections into the ischemic limbs, while the control group was injected with sterile saline and received conventional medical treatment. All patients were followed up after 12 weeks. At the end of the follow-up period, the main manifestations significantly improved in patients of the implanted group compared with the control group. The mean of rest pain decreased from the baseline level of 6.42?±?2.15 to 1.67?±?0.389 (P?<?0.001). The mean of pain-free walking distance increased from 25.00?±?8.90 to 409.00?±?104.00 (P?<?0.001). The mean ankle–brachial pressure index increased from 0.45?±?0.12 to 0.79?±?0.38 (P?=?0.005). Seven out of nine limb ulcers and wounds (77.8 %) of implanted patients healed after cell implantation. Two lower limb amputations (16.67 %) occurred in the implanted patients. In contrast, eight control patients (66.67 %) had to receive lower limb amputation. Implantation of stem/progenitor cells is a feasible and readily available effective strategy for therapeutic angiogenesis in patients with chronic limb ischemia.     

Intermittent arm ischemia induces vasodilatation of the contralateral upper limb

Intermittent arm ischemia before percutaneous coronary intervention induces remote ischemic preconditioning (RIPC) and attenuates myocardial injury in patients with myocardial infarction. Several studies have shown that intermittent arm ischemia increases coronary flow and is related to autonomic nerve system. The aim of this study was to determine whether intermittent arm ischemia induces vasodilatation of other arteries and to assess changes in the autonomic nerve system during intermittent arm ischemia in humans. We measured change in the right brachial artery diameter during intermittent left arm ischemia through three cycles of 5-min inflation (200 mmHg) and 5-min deflation of a blood-pressure cuff using a 10-MHz linear array transducer probe in 20 healthy volunteers. We simultaneously performed power spectral analysis of heart rate. Ischemia-reperfusion of the left arm significantly dilated the right brachial artery time-dependently, resulting in a 3.2 ± 0.4% increase after the 3rd cycle. In the power spectral analysis of heart rate, the high-frequency domain (HF), which is a marker of parasympathetic activity, was significantly higher after the 3rd cycle of ischemia-reperfusion than baseline HF (P = 0.02). Intermittent arm ischemia was accompanied by vasodilatation of another artery and enhancement of parasympathetic activity. Those effects may play an important role in the mechanism of RIPC.     

精胺减轻大鼠在体心肌缺血/再灌注损伤的作用及机制初探

目的: 观察低浓度外源性精胺对大鼠心肌缺血/再灌注损伤的影响。方法: Wistar大鼠随机分成假手术（Sham）组、缺血/再灌注损伤（I/R）组、盐水对照（NS）组和精胺干预（Sp）组（n=10）。结扎冠脉复制心肌缺血/再灌注损伤模型。Sp组缓慢静脉推注 0.5 mmol/L 精胺 2 mL/kg。观察指标：心电图，心功能参数，血清SOD、LDH、NO、MDA水平和心肌超微结构等。结果: I/R组心律失常发生率高达90％，心肌超微结构损伤严重，LVSP 和±dp/dtmax明显降低，血清中NO、MDA及LDH升高，SOD活性降低（P<0.05或P<0.01 vs Sham组）。Sp组与I/R组及NS组相比，上述指标均有显著差异（P<0.05或P<0.01）。结论: 低浓度外源性精胺能减轻大鼠心肌缺血/再灌注损伤，其机制可能与抗氧化和减轻氧自由基损伤有关。     

Soluble interleukin-2 receptor and interleukin-8 plasma levels during and after cardiopulmonary bypass: correlations with creatine kinase and creatine kinase MB

In this study, soluble receptor of interleukin-2, interleukin-8, creatine kinase, and creatine kinase MB isoenzyme levels were determined serially before, during, and after cardiopulmonary bypass in blood samples of 24 patients. Interleukin-2 receptor levels were 683±80 U/ml in the preoperative period and 640±60 U/ml during hyperthermia. Subsequently, these levels increased significantly at the end of the procedure (791±70 U/ml, P<0.01), remaining elevated 1 h after (882±92 U/ml, P<0.001) and reaching peak values 24 h postoperatively (1,752±200 U/ml, P<0.001). Preoperative plasma values of interleukin-8 were 230±43 pg/ml. Interleukin-8 concentrations were 185±25 pg/ml during hypothermia. The peak interleukin-8 levels were observed at the end of cardiopulmonary bypasss (754±94 pg/ml, P<0.001) and tended to decrease 1 h after the procedure (643±76 pg/ml, P<0.001), declining to preoperative values, 24 h postoperatively (273±41 pg/ml). Interleukin-2 receptor levels correlated well with creatine kinase levels during the procedure. Furhtermore, creatine kinase MB levels were correlated with interleukin-2 receptor values only at the end and 1 h after completion of cardiopulmonary bypass. We concluded that interleukin-8 and Interleukin-2 receptor levels are elevated after cardiopulmonary bypass and may contribute to myocardial injury as reflected by increased levels of creatine kinase and creatine kinase MB and correlations between interleukin-2 receptor and both creatine kinase and creatine kinase MB levels. Received: 17 July 2000 / Accepted: 12 February 2001     

Myocardial infarction quantification with late gadolinium-enhanced magnetic resonance imaging in rats using a 7-T scanner

AimsThe objective of this study was to noninvasively measure the volume of myocardial infarction in rats, using delayed enhancement magnetic resonance imaging (MRI) in a coronary occlusion/reperfusion model on a 7-T scanner.MethodsAt 24 h after cardiac ischemia, contrast-enhanced MRI was performed. Two distinct experimental groups were compared: one was subjected to permanent ischemia (PL) and the other was subjected to 30 min of ischemia followed by 24 h of reperfusion (IR). The sizes of enhanced regions were compared to triphenyltetrazolium chloride (TTC)-stained sections of the excised rat heart. Cardiomyocyte apoptosis was analyzed by TUNEL methods, and neutrophils and macrophages were quantitated after histology and immunohistochemical staining.ResultsTwenty-four hours after ischemia, delayed hyperenhancement imaging was clearly visualized in the anterior left ventricular walls corresponding to the infarcted myocardium. In the PL group, infarct size was 37.2±9.8% (LV %) as measured by MRI and 38.8±9% (LV %) by TTC (P=NS). In the IR group, infarct size was 23.2±8.8% (LV %) as measured by MRI and 24.4±9.2% (LV %) by TTC (P=NS). Infarction volume measured with MRI was strongly correlated to TTC staining (R=0.82 for PL, R=0.973 for IR). Increased inflammatory cell infiltration was detected in the infarct area of the heart after reperfusion compared to permanent ligation (P<.01). The ratio of TUNEL-positive cardiomyocytes to total number of cardiomyocytes in the IR group was significantly reduced as compared to the PL group (P<.01).ConclusionsMRI can accurately assess infarct size in intact rats early after MI. After transient arterial occlusion, the size of the myocardial infarct was found to be significantly smaller as compared to permanent occlusion.