Prolonged diastolic time fraction protects myocardial perfusion when coronary blood flow is reduced

Citation
D. Merkus et al., Prolonged diastolic time fraction protects myocardial perfusion when coronary blood flow is reduced, CIRCULATION, 100(1), 1999, pp. 75-81
Citations number
36
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
100
Issue
1
Year of publication
1999
Pages
75 - 81
Database
ISI
SICI code
0009-7322(19990706)100:1<75:PDTFPM>2.0.ZU;2-8
Abstract
Background-Because coronary blood flow is impeded during systole, the durat ion of diastole is an important determinant of myocardial perfusion. The ai m of this study was to show that coronary flow modulates the duration of di astole at constant heart rate. Methods and Results-In anesthetized, open-chest dogs, diastolic time fracti on (DTF) increased significantly when coronary flow was reduced by lowering perfusion pressure from 100 to 70, 55, and 40 mm Hg. On average, DTF incre ased 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 administrati on 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 (3 75 +/- 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 t o 0.22 +/- 0.06; and with L-NMMA, from 0.013 +/- 0.007 to 0.12 +/- 0.02 (al l P < 0.05). The increase in DTF at low pressure may be explained by a decr ease in interstitial volume at low pressure, which either decreases the pre load of the myocytes or reduces the buffer capacity for ions determining re polarization, thereby causing an earlier onset of relaxation. Conclusions-Because the largest increase in DTF occurs at pressures below t he autoregulatory range when blood flow to the subendocardium is closely re lated to DTF, modulation of DTF by coronary blood flow can provide an impor tant regulatory mechanism to match supply and demand of the myocardium when vasodilatory reserve is exhausted.