Armiger L C, Vanderwee M A, Fitzgerald S, Gavin J B, Herdson P B
Pathology. 1981 Apr;13(2):345-55. doi: 10.3109/00313028109081674.
An experimental model for producing a uniformly and maximally ischaemic segment of atrial myocardium has been devised and used in 23 dogs to investigate the effects of severe ischaemia of up to 6 h duration on the fine structure of atrial myocardial cells. Throughout the first 30 min of ischaemia the cells maintained a fine structure comparable with that of control tissue. In the subsequent 2 h they developed morphological alteration at differing rates, despite their uniform deprivation of blood supply. Even at 90 min the ischaemic tissue showed discontinuous change, with many areas differing little from control, and it was only after 3 h that all cells showed well developed and similar alterations. These included glycogen depletion, marked clumping and margination of nuclear chromatin, and the mitochondrial degeneration typically seen in ischaemically injured ventricle. The changes were very severe after 4 and 6 h of ischaemia, when disruption of cellular membrane systems was also evident. At these times the tissue closely resembled ventricular myocardium made ischaemic for similar intervals, except for the persistence of well-preserved 'specific atrial granules'. Atrial muscle cells therefore develop the fine structural changes associated with ischaemia more slowly than ventricular muscle cells and have a more variable response to the initiation of ischaemic injury.
已经设计出一种用于产生心房心肌均匀且最大程度缺血节段的实验模型，并将其应用于23只犬，以研究长达6小时的严重缺血对心房心肌细胞超微结构的影响。在缺血的最初30分钟内，细胞保持与对照组织相当的超微结构。在随后的2小时内，尽管它们的血液供应均被剥夺，但它们以不同的速率发生形态学改变。即使在90分钟时，缺血组织也显示出不连续的变化，许多区域与对照差异不大，并且只有在3小时后所有细胞才显示出充分发展且相似的改变。这些改变包括糖原耗竭、核染色质明显凝集和边缘化，以及在缺血性损伤的心室中典型见到的线粒体变性。在缺血4小时和6小时后，这些变化非常严重，此时细胞膜系统的破坏也很明显。在这些时候，除了保存完好的“特异性心房颗粒”持续存在外，该组织与缺血相似时间的心室心肌非常相似。因此，心房肌细胞比心室肌细胞更缓慢地发生与缺血相关的超微结构变化，并且对缺血性损伤的起始反应更具变异性。
