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In order to determine the distribution pattern of digoxin in infarcted and ischemic tissue, the early uptake of tritiated digoxin ( 3 H-digoxin) in the acutely and chronically infarcted canine left ventricle (LV) was studied. Seven open-chest anesthetized dogs were given 3 H-digoxin intravenously 1 hour following acute anterior-wall infarction produced by serial coronary arterial branch ligations. Central and peripheral zones of infarction, ischemic border zones, and nonischemic myocardium were demarcated by epicardial electrode mapping. Two hours after 3 H-digoxin administration, animals were sacrificed and epicardial and endocardial samples from each zone were analyzed for 3 H-digoxin uptake. Significantly lower digoxin concentrations (ng/g wet weight ± ( sem ) were found in both endocardial (endo) and epicardial (epi) regions of the center (endo 27 ± 11; epi 58 ± 10) and periphery (endo 51 ± 13; epi 112 ± 13) of the infarct as compared to the border (endo 217 ± 21; epi 242 ± 15) and nonischemic (endo 256 ± 22; epi 220 ± 20) zones. Significant transmural gradients of the glycoside observed in infarct zones (endo/epi ratio 0.46) were the reverse of those found in nonischemic portions of the myocardium (endo/epi ratio 1.16). Four dogs with chronic infarcts showed 3 H-digoxin uptake patterns similar to acutely infarcted animals. In four sham-operated dogs, 3 H-digoxin uptake was homogeneous in all areas of the LV. This marked alteration of early 3 H-digoxin uptake by the infarcted LV may predispose to electrical instability and the genesis of ectopic rhythm disturbances. The pattern of LV digoxin uptake appears to reflect, at least in part, regional blood flow to infarcted, ischemic, and nonischemic tissue.
Beller et al. (1972) studied this question.