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AJP - Heart and Circulatory Physiology, Vol 257, Issue 4 1184-H1191, Copyright © 1989 by American Physiological Society
ARTICLES |
P. A. Gayheart, J. Vinten-Johansen, W. E. Johnston, T. O. Hester and A. R. Cordell
Department of Physiology, Bowman Gray School of Medicine, Wake Forest University Medical Center, Winston-Salem, North Carolina 27103.
Oxygen requirements of a noncontracting myocardial segment subjected to passive systolic stretch (dyskinesis) have not been well described. The purpose of this study was to measure oxygen consumption (MVO2) of a myocardial segment made dyskinetic by intracoronary infusion of lidocaine. In 12 anesthetized open-chest dogs, segmental shortening was measured sonomicrometrically in regions perfused by the left anterior descending (LAD) and circumflex (Cfx) coronary arteries. MVO2 was measured by arterial-venous oxygen content differences and transmural blood flow. Dose-response curves to intracoronary lidocaine showed that complete dyskinesis was achieved by a 0.25-mg/ml dose of lidocaine, whereas the Cfx region maintained a constant level of segmental shortening. MVO2 of the LAD segment was similar to that of the Cfx segment under control conditions. With lidocaine-induced dyskinesis, MVO2 in the arrested segment was reduced by 33% (P less than 0.05), despite the loss of contractile function. When bulging was prevented by ventricular unloading, MVO2 in the arrested segment decreased to 2.65 ml O2.min-1.100 g-1 (i.e., basal oxygen requirements). In conclusion, MVO2 in a pharmacologically arrested myocardial segment undergoing systolic bulging is paradoxically high relative to both basal requirements and MVO2 in the normally contracting segment.
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