Abstract
Summary
Following surgical myocardial infarction in dogs, a marked decline in cardiac norepinephrine stores has been observed. In an attempt to elucidate the mechanism of the NE-depletion, the uptake, degradation, and subcellular distribution of norepinephrine in the canine myocardium were determined after myocardial infarction. The subcellular distribution, uptake and accumulation of tracer doses of dl-norepinephrine-7-14C were unchanged and the rate of degradation was not significantly increased. It appears thus, that the decline in cardiac norepinephrine stores following infarction is neither due to a decreased ability of the sympathetic nerve ending to take up and accumulate NE, nor to an increased rate of degradation.
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