Armiger L C, Knell C M
J Mol Cell Cardiol. 1986 Oct;18 Suppl 4:11-5. doi: 10.1016/s0022-2828(86)80019-0.
The fine structural effects of oxygen deficiency on the cardiac conduction system were studied in the dog and the rat, using various in vitro and in vivo models. Observations did not support the concept that conducting cells are inherently more resistant to ischaemia and anoxia than contractile myocardial cells. Nodal cells altered more rapidly than His-Purkinje cells in the dog, but not in the rat, which has less clearly-defined cell differences in these regions and a greater glycogen content in the atrioventricular node. Cellular alteration was uniform in global ischaemia in the isolated rat heart, but focal in high-flow, glucose-free anoxia. Comparison of in vitro and in vivo observations in the dog indicated that better collateral blood flow is chiefly responsible for preservation of conducting elements in the context of myocardial infarction.
利用各种体外和体内模型，研究了缺氧对犬和大鼠心脏传导系统的精细结构影响。观察结果不支持传导细胞比收缩性心肌细胞天生更耐缺血和缺氧这一观点。在犬中，结细胞比希氏 - 浦肯野细胞变化更快，但在大鼠中并非如此，大鼠在这些区域的细胞差异不太明显，且房室结中的糖原含量更高。在离体大鼠心脏的全脑缺血中，细胞变化是均匀的，但在高流量、无糖缺氧中是局灶性的。犬的体外和体内观察结果比较表明，更好的侧支血流是心肌梗死情况下传导元件得以保存的主要原因。
