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AJP - Heart and Circulatory Physiology, Vol 256, Issue 6 1645-H1650, Copyright © 1989 by American Physiological Society
ARTICLES |
N. Sadick, G. P. Dube, P. A. McHale and J. C. Greenfield Jr
Department of Medicine, Duke University Medical Center, Durham 27710.
This study determined whether the reactive hyperemic response to a 400-ms diastolic coronary occlusion is dependent on ventricular systole. Studies were obtained on 11 conscious dogs with complete heart block paced at 60 beats/min. A pressure catheter was chronically implanted in the aorta. An electromagnetic flow probe and pneumatic occluder were implanted on the circumflex coronary artery. Three interventions were employed: 1) interruption of pacing for a single beat generating a long diastolic period of 2,000 ms in duration (LDC); 2) introduction of a 400-ms diastolic coronary occlusion early in a long diastole (LD4); and 3) a 400-ms diastolic occlusion during uninterrupted pacing (400R). The rise in diastolic coronary vascular resistance index noted during LDC was inhibited significantly in the last 600 ms of diastole during LD4. Thus an intervening systole is not required for a reactive hyperemic response to a diastolic coronary occlusion. During 400R, the resistance index was lower than that found during LD4. The reactive hyperemic response may be caused by either a myogenic or metabolic mechanism or by both. The greater vasodilatation observed after the postocclusion systole in 400R probably reflects metabolic influences.
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