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pubmed:abstractText |
This study evaluated alterations in catecholamines, blood flow, and indices of tissue damage during early myocardial ischemia in the dog. Of the 27 animals studied, the left anterior descending artery was ligated for 1 hour in 11 and for 3 hours in 13, and 3 underwent sham procedures. The severity of ischemia was determined by the radioactive microsphere and thioflavin S techniques. Myocardial catecholamines were measured radioenzymatically, and catecholamine-containing nerve terminals were visualized histochemically and quantitated with the use of a point-counting method. After both 1- and 3-hour occlusions, there was a greater reduction in catecholamine-containing nerve terminals than in total tissue catecholamines in ischemic tissue. In both ischemic and nonischemic tissue, the relative percentages of total catecholamines as norepinephrine, dopamine, and epinephrine were similar. In the dogs with 3-hour occlusions, values (as a percentage of control values) for total tissue catecholamines were 83% in ischemic subepicardium and 76% in ischemic subendocardium, whereas values for catecholamine-containing nerve terminals were 58% and 51%, respectively. (Only the latter three values were significantly different from control values by analysis of variance). Diffusion of catecholamines from the nerve terminals frequently was noted in the ischemic areas, and degenerative changes in nerve terminals were demonstrated by electron microscopy in 2 animals. These data indicate that catecholamines, primarily as norepinephrine, are released from nerve terminals and accumulate in another tissue compartment in the ischemic myocardium. Quantitative light microscopy showed significant myocyte damage after 1 hour of ischemia in the subendocardium, although not in the subepicardium. There was significant damage in the subepicardium and subendocardium after 3 hours of ischemia. Thus, ischemic injury is associated with the redistribution and abnormal localization of catecholamines in ischemic myocardium, and these phenomena occur during the transmural spread of necrosis in evolving myocardial infarction.
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