AJP - Heart and Circulatory Physiology, Vol 259, Issue 4 1190-H1196, Copyright © 1990 by American Physiological Society
Myocardial high-energy phosphates in reactive hyperemia
G. G. Schwartz, S. Schaefer, J. Gober, D. J. Meyerhoff, A. Smekal, B. Massie and M. W. Weiner
Magnetic Resonance Unit, Veterans Administration Medical Center, San Francisco, California.
This study used 31P nuclear magnetic resonance (NMR) spectroscopy to
determine whether the magnitude and duration of myocardial reactive
hyperemia (RH) reflect a commensurate derangement of myocardial high-energy
phosphate (HEP) metabolism, or if coronary blood flow (CBF) and HEP
metabolism are dissociated during RH. Twelve open-chest anesthetized pigs
were studied during and after 24 s occlusion of the anterior descending
coronary artery. CBF velocity was measured with a Doppler probe. NMR time
resolution (4.8 s) was obtained by summing corresponding short blocks of
data from multiple occlusions. During occlusion, phosphocreatine (PCr)
declined to 65 +/- 5% (mean +/- SE) of control accompanied by increased
spectral intensity of the Pi + phosphomonester region. By 20 s of reflow,
HEPs had returned to control levels, but CBF was still elevated at 282 +/-
18% of control and remained elevated for an additional 53 +/- 7 s, during
which 44 +/- 6% of total RH flow occurred. Therefore, the control of CBF is
not closely coupled to the levels of myocardial HEPs during RH and the
duration of RH does not reflect prolonged depletion of myocardial HEPs.
