This study investigates the histochemical correlation between potassium and glycogen distribution in areas adjacent to myocardial infarcts to explore a potential physioanatomic basis for these alterations.
Hypothesis-generating in animal models; leaves open any clinical relevance for post-MI histochemistry.
Evidence is accumulating that potassium and glycogen are closely related biochemically. Feuiui (3) has shown that the deposition of hepatic glycogen is accompanied by potassium and water. In vitro studies of liver have shown that synthesis of glycogen from glucose is greater in media high in potassium (2, 7). The shift of glucose accompanied by potassium from the blood into the liver in treated diabetics has been well documented (8). In contrast, in vitro studies using skeletal muscle and heart have suggested that glycogen synthesis is en-hanced by media low in cation content (19, 20). The indispensability of potassium in the trans-phorylation of phosphopyruvate with adenosine tn-phosphate has been shown (1) and confirmed (16). Pathologic deposits of glycogen accumulate around the borders of myocardial infarcts (21), particularly along the suhendocardium.1 During the past two years we have attempted to correlate the distribution of glycogen and potassium in these areas adjacent to myocardial infarcts in view of the possibility that zonal alterations of potassium and glycogen might be a physioanatomic basis for the
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POPPEN et al. (1953) studied this question.
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