Structural alterations in cardiac conducting cells in oxygen deficiency.
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.
D000818:Animals; D001283:Atrioventricular Node / Q000648:ultrastructure; D003327:Coronary Disease / Q000473:pathology*; D004285:Dogs; D006329:Heart Conduction System / Q000648:ultrastructure*; D000860:Hypoxia / Q000473:pathology*; D008929:Mitochondria, Heart / Q000648:ultrastructure; D011690:Purkinje Fibers / Q000648:ultrastructure; D051381:Rats; D013045:Species Specificity