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Effect of Rate on Changes in Conduction Velocity and Extracellular Potassium Concentration During Acute Ischemia in the In Situ Pig Heart
Author(s) -
HARPER JAMES R.,
JOHNSON TIMOTHY A.,
ENGLE CONNIE L.,
MARTIN DAVID G.,
ELEET WILLIAM,
GETTES LEONARD S.
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.tb01252.x
Subject(s) - medicine , ischemia , nerve conduction velocity , cardiology , potassium , thermal conduction , heart rate , anesthesia , coronary occlusion , stimulation , fissipedia , chemistry , blood pressure , materials science , organic chemistry , composite material
Rate Effects on Conduction and [K + ] e During Ischemia. Introduction: The purpose nf our study was to determine if the slowing oflongitudinal intraventricular conduction in the in situ porcine heart during acute regional no‐flow ischemia was rate dependent. Further, we investigated whether any rate dependence could he correlated to a rate‐dependent component of the ischemiainduced rise in extracellular potassium concentration. [K + ] e . Methods and Results: We studied in situ hearts in nine anesthetized open chest pigs in which acute no‐flow ischemia was induced by occlusion of the left anterior descending coronary artery. To determine the effects of steady‐state rate on the slowing of conduction and rise in [K + ] e during ischemia, we varied the rate of stimulation during sequential occlusions from 90 to 150 beats/min. Longitudinal conduction velocity was determined by unipolar electrodes embedded in a plaque that was sutured to the epicardial surface in the center of the ischemic zone. Myocardial [K + ] e was determined simultaneously by potassium‐sensitive electrodes placed at or within 1 to 2 mm of the epicardium in close proximity to the activation recording electrodes. Conduction vehxity decreased more rapidly at the more rapid rates of stimulation although the reduction in conduction velocity occurring prior to the onset of conduction block was similar at both rates. The potassium change was not rate dependent and rose at the same rate regardless of the rate of stimulation. Conclusion: Our study demonstrates that the steady‐state rate‐dependent component of the slowing of intraventricular conduction induced by acute ischemia in the in situ porcine heart occurs in the absence of a rate‐dependent component in the rise of [K + ] e . Between rates of 90 and 150 beats/min, the rate dependence of the conduction slowing may be attributed to one or more potassium‐independent factors such as the rate‐dependent changes in resting membrane potential, in V̇ max of the action potential upstroke, and in cell‐to‐cell uncoupling, which have hcen observed in other models of acute ischemia.