In an in situ porcine model of acute ischemia, the steady-state rate-dependent component of intraventricular conduction slowing occurred without a rate-dependent component in the rise of extracellular potassium.
In an in situ pig heart model of acute ischemia, the rate-dependent slowing of intraventricular conduction occurs independently of changes in extracellular potassium concentration.
INTRODUCTION: The purpose of our study was to determine if the slowing of longitudinal 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 be correlated to a rate-dependent component of the ischemia-induced 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 velocity 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 Vmax of the action potential upstroke, and in cell-to-cell uncoupling, which have been observed in other models of acute ischemia.
HARPER et al. (Wed,) conducted a other in Acute regional no-flow ischemia (n=9). Variation of stimulation rate (90 to 150 beats/min) was evaluated on Rate dependence of slowing of longitudinal intraventricular conduction and rise in extracellular potassium concentration ([K+]e). In an in situ porcine model of acute ischemia, the steady-state rate-dependent component of intraventricular conduction slowing occurred without a rate-dependent component in the rise of extracellular potassium.