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

被引:56
作者
Merkus, D
Kajiya, F
Vink, H
Vergroesen, I
Dankelman, J
Goto, M
Spaan, JAE
机构
[1] Univ Amsterdam, Acad Med Ctr, Cardiovasc Res Inst Amsterdam, Dept Phys Med, NL-1105 AZ Amsterdam, Netherlands
[2] Delft Univ Technol, Lab Measurement & Control, Fac Design Engn & Prod Mech Engn & Marine Technol, Delft, Netherlands
[3] Kawasaki Med Sch, Dept Med Engn & Syst Cardiol, Okayama, Japan
关键词
diastole; metabolism; circulation; perfusion; contractility;
D O I
10.1161/01.CIR.100.1.75
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:75 / 81
页数:7
相关论文
共 36 条
[1]   ENHANCEMENT OF LEFT-VENTRICULAR RELAXATION IN THE ISOLATED HEART BY AN ANGIOTENSIN-CONVERTING ENZYME-INHIBITOR [J].
ANNING, PB ;
GROCOTTMASON, RM ;
LEWIS, MJ ;
SHAH, AM .
CIRCULATION, 1995, 92 (09) :2660-2665
[2]  
[Anonymous], CORONARY ARTERY STEN
[3]   ENERGY-METABOLISM AND CONTRACTILE FUNCTION AFTER 15 BEATS OF MODERATE MYOCARDIAL-ISCHEMIA [J].
ARAI, AE ;
PANTELY, GA ;
THOMA, WJ ;
ANSELONE, CG ;
BRISTOW, JD .
CIRCULATION RESEARCH, 1992, 70 (06) :1137-1145
[4]   PERSISTENCE OF CORONARY VASODILATOR RESERVE DESPITE FUNCTIONALLY SIGNIFICANT FLOW REDUCTION [J].
AVERSANO, T ;
BECKER, LC .
AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 248 (03) :H403-H411
[5]   EFFECT OF MAXIMAL CORONARY VASODILATION ON TRANSMURAL MYOCARDIAL PERFUSION DURING TACHYCARDIA IN AWAKE DOG [J].
BACHE, RJ ;
COBB, FR .
CIRCULATION RESEARCH, 1977, 41 (05) :648-653
[6]  
Brutsaert D L, 1988, Adv Exp Med Biol, V226, P609
[7]   REDUCED REGIONAL MYOCARDIAL PERFUSION IN THE PRESENCE OF PHARMACOLOGIC VASODILATOR RESERVE [J].
CANTY, JM ;
KLOCKE, FJ .
CIRCULATION, 1985, 71 (02) :370-377
[8]   EFFECT OF ISCHEMIA AND ROLE OF EICOSANOIDS IN RELEASE OF ATRIAL-NATRIURETIC-FACTOR FROM RAT-HEART [J].
CHEN, BN ;
RAYNER, TE ;
MENADUE, MF ;
MCLENNAN, PL ;
OLIVER, JR .
CARDIOVASCULAR RESEARCH, 1993, 27 (09) :1576-1579
[9]   REDISTRIBUTION OF CORONARY MICROVASCULAR RESISTANCE PRODUCED BY DIPYRIDAMOLE [J].
CHILIAN, WM ;
LAYNE, SM ;
KLAUSNER, EC ;
EASTHAM, CL ;
MARCUS, ML .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 256 (02) :H383-H390
[10]   DOES SYSTOLIC SUBEPICARDIAL PERFUSION COME FROM RETROGRADE SUBENDOCARDIAL FLOW [J].
FLYNN, AE ;
COGGINS, DL ;
GOTO, M ;
ALDEA, GS ;
AUSTIN, RE ;
DOUCETTE, JW ;
HUSSEINI, W ;
HOFFMAN, JIE .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (06) :H1759-H1769