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Rapid Inward Current in Ischemically‐Injured Subepicardial Myocytes Bordering Myocardial Infarction
Author(s) -
PATTERSON EUGENE,
SCHERLAG BENJAMIN J.,
LAZZARA RALPH
Publication year - 1993
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1993.tb01208.x
Subject(s) - myocyte , medicine , collagenase , cardiology , myocardial infarction , electrophysiology , membrane potential , refractory period , infarction , endocrinology , biophysics , chemistry , biology , biochemistry , enzyme
Ischemically‐Injured Myocytes. Introduction: To determine if collagenase‐dispersed epicardial myocytes overlying myocardial infarction reproduce the same altered electrophysiology observed in intact epicardiuma, multicellular tissue preparations and enzymatically‐dispersed myocytes from ischemically‐injured canine subepicardium were examined 1 and 4 days after myocardial infarction. Methods and Results: The electrophysiologica changes observed with alchemic injury in enzymatic ally‐dispersed myocytes were not different from changes observed in multicellular tissue preparations at I and 4 days post infarction. Is chemically‐injured myocytes were depolarized versus normal myocytes at [K 0 ] (2.5 to 40 mM) with reduced membrane potentials also observed in injured subepicardial tissue preparations [K] (4 to 24 mM). On day 1, the reduced V max and the prolonged recovery of V max from inactivation were consistent with the reduced membrane potentials observed at each [K] + . The half‐maximal V max , maximal V max and Boltzmann constant (k) in injured myocytes were unchanged versus normal myocytes. On day 4 postinfarction, the half‐maximal V max was shifted to a more negative membrane potential, the maximal V max . was reduced, and k was increased in injured versus normal myocytes. Prolonged recovery from inactivation was observed with depressed membrane potentials in injured myocytes on day 4. Conclusion: Enzymatically‐dispersed myocytes from ischemically‐injured subepicardium closely reproduce altered cellular properties observed in multicellular tissue preparations. The data suggest that 1 day postinfarction, altered conduction and refractoriness largely result from a reduced membrane potential. At 4 days, a reduced maximal V max a shift in the inactivation curve to more negative voltages, and prolonged recovery of V max , from inactivation also contribute to slowed conduction and prolonged refractoriness.