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Prolonged Diastolic Time Fraction Protects Myocardial Perfusion When Coronary Blood Flow Is Reduced

Prolonged Diastolic Time Fraction Protects Myocardial Perfusion When Coronary Blood Flow Is Reduced,Daphne Merkus,Fumihiko Kajiya,Hans Vink,Isabelle V

Prolonged Diastolic Time Fraction Protects Myocardial Perfusion When Coronary Blood Flow Is Reduced   (Citations: 18)
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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 0.4760.04 to 0.5560.03 after a pressure step from 100 to 40 mm Hg in control, from 0.4260.04 to 0.4760.04 after administration of adenosine, and from 0.4660.07 to 0.5560.06 after L-NMMA (mean6SD, 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 (375625 mL/min) increased during the period of reduced pressure at 40 mm Hg; control, from 0.005663 (2 seconds after pressure step) to 0.0960.06 (15 seconds after pressure step); with adenosine, from 0.1960.06 to 0.2260.06; and with L-NMMA, from 0.01360.007 to 0.1260.02 (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. (Circulation. 1999;100:75-81.)
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