Infarct size and nitric oxide synthase in murine myocardium
Infarct size and nitric oxide synthase in murine myocardium
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DOI：
10.1006/jmcc.1999.1050
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发表时间：
2000-01-01
影响因子：
5
通讯作者：
Yellon, DM
中科院分区：
文献类型：
--
作者：
Sumeray, MS;Rees, DD;Yellon, DM
围绕一氧化氮(NO)在心肌缺血-再灌注损伤中的作用以及有害和有益之间的平衡存在争议。一氧化氮合酶(NOS)有两种亚型：内皮型(ENOS)和神经型(NNOS)。缺乏eNOS(ENOS KO)或nNOS(NNOS KO)基因的基因敲除小鼠与野生型(WT)在全脑缺血再灌注损伤过程中进行了比较。分离小鼠心脏36只(每组12只)，用改良的Krebs液在恒压下经主动脉置管，用心尖缝线将左心室与力传感器通过轻质联轴器相连。在心脏稳定后，在37℃下进行30min的整体缺血，在30min的再灌流期间，记录基线力率乘积(F%)的恢复。心脏随后被四氮唑染色，冷冻，切片，并与福尔马林融合。切片在有机玻璃平板之间被压缩，放大的视频图像被数字化以允许平面测量梗死大小(以脑室体积I/R的百分比表示)。尽管eNOSKO组的收缩功能恢复无差异，但eNOSKO组的心肌梗死面积明显大于WT组和nNOSKOS组(分别为41vs33和30%，P
Controversy surrounds the involvement of nitric oxide (NO) in myocardial ischaemia-reperfusion injury and the balance between deleterious and beneficial effects. NO synthase (NOS) is expressed constitutively as two isoforms: endothelial (eNOS) and neuronal (nNOS). Knockout mice lacking the gene for either eNOS (eNOS KO) or nNOS (nNOS KO), were compared with wild-types (WT) during a protocol of global ischaemia-reperfusion injury. Thirty-six mouse hearts (12 from each group) were isolated and the aorta cannulated for Langendorff perfusion with modified Krebs solution at constant pressure, An apical suture connected the left ventricle to a force transducer via a light weight coupling rod. Following stabilization hearts were subjected to 30 min of global ischaealia at 37 degrees C. During 30 min reperfusion, the recovery of baseline force-rate product (F%) was recorded. Hearts were then stained with tetrazolium, frozen, sliced, and Futed with formalin. Slices were compressed between plexiglas plates, and a magnified video image digitized to allow planmetry for infarct size (as percentage of ventricular volume I/R). Although recovery of contractile function did not differ between groups, eNOS KOs suffered significantly larger infarcts than WT or nNOS KOs (41 v 33 and 30% respectively, P