This preclinical study characterizes the rapid shifts in electrolytes, water, and catecholamines within infarcted myocardium following acute coronary occlusion.
These early post-infarct shifts extend preclinical models of ischemic injury; leaves open human translation and therapeutic relevance.
Myocardial infarction was produced by ligation of the coronary artery in a series of 20 dogs, which were killed 1, 4 1/2, 12, or 24 hours later. Each heart was divided into three parts: the infarcted area, the undamaged area, and a border zone including some of each. Each part was analyzed for its content of sodium, potassium, epinephrine, norepinephrine, and water. The water content of the infarct is detectably higher within 1 hour, reaching its ultimate concentration more rapidly than do the other changes seen. Potassium is lost from the infarct and replaced by sodium. The catecholamines progressively decrease in concentration within the infarct during the first 24 hours. No evidence of selective accumulation or loss of any of these constituents in the border zone was noted, although this zone appears to trigger the ventricular arrhythmia that occurs after coronary occlusion. The possible roles of potassium, epinephrine, and norepinephrine, as agents excitatory to such tachycardia, are discussed.
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Russell et al. (1961) studied this question.
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