Effect of rate on changes in conduction velocity and extracellular potassium concentration during acute ischemia in the in situ pig heart.
BACKGROUND
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.


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.


CONCLUSIONS
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
J R
JR
Division of Cardiology, University of North Carolina, Chapel Hill 27599.
Johnson
T A
TA
Engle
C L
CL
Martin
D G
DG
Fleet
W
W
Gettes
L S
LS
D000200:Action Potentials / Q000502:physiology; D000208:Acute Disease; D000818:Animals; D001692:Biological Transport / Q000502:physiology; D002462:Cell Membrane / Q000502:physiology / Q000648:ultrastructure; D005110:Extracellular Space / Q000737:chemistry*; D006329:Heart Conduction System / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D008564:Membrane Potentials / Q000502:physiology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000737:chemistry* / Q000473:pathology* / Q000648:ultrastructure; D011188:Potassium / Q000032:analysis* / Q000097:blood / Q000493:pharmacokinetics; D013552:Swine / Q000502:physiology*; D013997:Time Factors
D011188:Potassium