(Circulation. 1999;100:75-81.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Prolonged Diastolic Time Fraction Protects Myocardial Perfusion When Coronary Blood Flow Is Reduced
From the Department of Medical Physics, Cardiovascular Research Institute Amsterdam, Academic Medical Center, University of Amsterdam (D.M., H.V., I.V., J.A.E.S.), and the Faculty of Design, Engineering and Production, Mechanical Engineering and Marine Technology, Laboratory for Measurement and Control, Delft University of Technology (J.D.), Netherlands; and the Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Okayama, Japan (F.K., M.G.).
Correspondence to Prof Dr Ir J.A.E. Spaan, Department of Medical Physics, Cardiovascular Research Institute Amsterdam, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, PO Box 22700, 1100 DE Amsterdam, Netherlands. E-mail j.a.spaan{at}amc.uva.nl
Background—Because coronary blood flow is impeded during systole, the duration of diastole is an important determinant of myocardial perfusion. The aim of this study was to show that coronary flow modulates the duration of diastole at constant heart rate.
Methods and Results—In anesthetized, open-chest dogs, diastolic time fraction (DTF) increased significantly when coronary flow was reduced by lowering perfusion pressure from 100 to 70, 55, and 40 mm Hg. On average, DTF increased from 0.47±0.04 to 0.55±0.03 after a pressure step from 100 to 40 mm Hg in control, from 0.42±0.04 to 0.47±0.04 after administration of adenosine, and from 0.46±0.07 to 0.55±0.06 after L-NMMA (mean±SD, 6 dogs for control and adenosine, 4 dogs for L-NMMA, all P<0.05). Flow normalized to its value at full dilation and pressure of 90 mm Hg (375±25 mL/min) increased during the period of reduced pressure at 40 mm Hg; control, from 0.005±63 (2 seconds after pressure step) to 0.09±0.06 (15 seconds after pressure step); with adenosine, from 0.19±0.06 to 0.22±0.06; and with L-NMMA, from 0.013±0.007 to 0.12±0.02 (all P<0.05). The increase in DTF at low pressure may be explained by a decrease in interstitial volume at low pressure, which either decreases the preload of the myocytes or reduces the buffer capacity for ions determining repolarization, thereby causing an earlier onset of relaxation.
Conclusions—Because the largest increase in DTF occurs at pressures below the autoregulatory range when blood flow to the subendocardium is closely related to DTF, modulation of DTF by coronary blood flow can provide an important regulatory mechanism to match supply and demand of the myocardium when vasodilatory reserve is exhausted.
Key Words: diastole • metabolism • circulation • perfusion • contractility
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