The relationship between coronary perfusion pressure, flow, and resistance in stenosed human coronary arteries: The critical importance of small changes in % stenosis

1974 ◽  
Vol 33 (1) ◽  
pp. 153 ◽  
Author(s):  
Samuel E. Logan ◽  
John V. Tyberg ◽  
William W. Parmley ◽  
H.J.C. Swan
Keyword(s):  
Coronary Arteries ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Critical Importance ◽  
Pressure Flow ◽  
The Relationship

Inorganic phosphate and coronary perfusion pressure mediate contractile dysfunction during mild ischemia

1997 ◽  
Vol 273 (2) ◽  
pp. H566-H572 ◽  
Author(s):  
M. Miyamae ◽  
S. A. Camacho ◽  
W. D. Rooney ◽  
G. Modin ◽  
H. Z. Zhou ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Atp Hydrolysis ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Resonance Spectroscopy ◽  
Coronary Perfusion ◽  
Contractile Dysfunction ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
The Relationship

During mild graded ischemia in perfused rat hearts, we (V.M. Figueredo, R. Brandes, M. W. Weiner, B. M. Massie, and S. A. Camacho. J. Clin. Invest 90: 1794-1802, 1992) previously found a relationship between decreased left ventricular developed pressure (LVDP) and increased Pi, in which intracellular pH, cytosolic Ca2+ concentration ([Ca2+]i), ATP, and free-energy change of ATP hydrolysis were not altered enough to affect contractility. However, the contribution of decreased coronary perfusion pressure (CPP) to decreased LVDP could not be determined. Thus, in the present study, graded hypoxia in perfused rat hearts (95-37.5% O2) was used to increase Pi to similar levels produced during mild ischemia without altering CPP and minimizing changes of other potential mediators of contractile dysfunction. 31P-magnetic resonance spectroscopy and indo 1 fluorescence were used to assess energy metabolites and [Ca2+]i, respectively. The relationship between LVDP and Pi during graded hypoxia was fit to a monoexponential (LVDP = 105 x e-0.04Pi). These data were compared with the relationship of LVDP and Pi during mild ischemia (LVDP = 106 x e-0.08Pi) (V. M. Figueredo, R. Brandes, M. W. Weiner, B. M. Massie, and S. A. Camacho. J. Clin. Invest 90: 1794-1802, 1992). The exponential constant, which describes the effect of Pi on LVDP, was 50% lower during graded hypoxia relative to mild ischemia. This suggests that another mediator, which accounted for approximately 50% of the decrease of LVDP during mild ischemia, was not present during hypoxia. Because CPP decreased during ischemia but not hypoxia, these data suggest that CPP and Pi contribute similarly in mediating contractile dysfunction during mild ischemia.

Pressure-flow characteristics of the coronary collaterals: a model study

1994 ◽  
Vol 266 (1) ◽  
pp. H310-H318 ◽  
Author(s):  
D. Manor ◽  
R. Beyar ◽  
S. Sideman
Keyword(s):  
Perfusion Pressure ◽  
Flow Characteristics ◽  
Coronary Perfusion Pressure ◽  
Back Pressure ◽  
Coronary Perfusion ◽  
Collateral Flow ◽  
Retrograde Flow ◽  
Pressure Flow ◽  
Coronary Collaterals ◽  
Wide Range

The pressure-flow relationship of the coronary collaterals is investigated by using an electrical analog model that combines the coronary epicardial arteries with the nonlinear characteristics of the intramyocardial circulation. The study aims to examine some controversial issues concerning the collateral circulation, including the transmural distribution of the collaterals, the distensibility of the collateral vessels (whether rigid or complaint), the effects of microcirculatory embolization, the collateral zero-flow pressure, and the nonlinearity of the collateral pressure-flow relationship. The study is carried out by simulating and comparing two basic experimental set-ups in which a coronary artery is ligated and the retrograde flow serves as an index of collateral flow. In the first “free-flow” setup, flow is allowed to bleed retrogradely against atmospheric pressure while perfusion pressure to the rest of the coronary arteries is varied over a wide range. In the second “back-pressure” setup, the coronary perfusion pressure is maintained at the control levels while the back pressure to the retrograde flow in the excised artery is varied. According to the analysis, the nonlinear pressure-flow relationships depend heavily on the experimental setup and are a function of the distensibility of the collaterals, which are distributed mainly on the epicardial surface, and the nonlinear contraction characteristics of the myocardium. The measured retrograde flow tends to underestimate the total collateral flow for the back-pressure setup because of antegrade flow escape.

Coronary pressure-flow autoregulation protects myocardium from pressure-induced changes in oxygen consumption

1994 ◽  
Vol 266 (6) ◽  
pp. H2359-H2368 ◽  
Author(s):  
X. J. Bai ◽  
T. Iwamoto ◽  
A. G. Williams ◽  
W. L. Fan ◽  
H. F. Downey
Keyword(s):  
Oxygen Consumption ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Coronary Perfusion ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Anesthetized Dogs ◽  
Induced Changes

Pressure-flow autoregulation minimizes changes in coronary blood flow (CBF) when coronary perfusion pressure (CPP) is altered. This investigation determined if autoregulation also minimizes CPP-induced changes in coronary vascular volume (CVV) and CVV-dependent changes in myocardial oxygen consumption (MVO2). In 11 anesthetized dogs, the left anterior descending coronary artery was cannulated, and responses to 20-mmHg changes in CPP were examined over a range of CPP from 60 to 180 mmHg. Changes in CPP had no significant effect on systemic hemodynamics or on left ventricular end-diastolic segment length, end-systolic segment length, or percent segment shortening. In hearts with effective pressure-flow autoregulation [closed-loop gain (GC) > 0.4], CVV increased 0.06%/mmHg change in CPP. For the same hearts, MVO2 increased 0.04%/mmHg change in CPP. In hearts with ineffective autoregulation (GC < 0.4), CVV increased 0.97%/mmHg (P < 0.001 vs. autoregulating hearts), and MVO2 increased 0.41%/mmHg (P < 0.001 vs. autoregulating hearts). MVO2 and CVV were correlated (r = 0.69, P < 0.0001) independently of autoregulatory capability, but only when autoregulation was poor and capacitance was elevated did CPP significantly affect MVO2. We conclude that pressure-flow autoregulation protects myocardium from CPP-induced changes in CVV, which in turn produces changes in oxygen consumption.

Downward shift of coronary pressure-flow relationship following a brief period of ischemia in dogs

1995 ◽  
Vol 269 (4) ◽  
pp. H1237-H1245
Author(s):  
T. Morioka ◽  
M. Kitakaze ◽  
T. Minamino ◽  
S. Takashima ◽  
K. Node ◽  
...  
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Downward Shift ◽  
Myocardial Contractile ◽  
Hyperemic Flow ◽  
Fractional Shortening

This study was undertaken to test whether a brief period of ischemia affects the coronary pressure-flow relationship during reduction of coronary perfusion pressure (CPP). The left anterior descending coronary artery was cannulated and perfused with blood from the left carotid artery in 40 open-chest dogs. Coronary blood flow (CBF) was measured during intracoronary administrations of papaverine and adenosine. The coronary pressure-flow relationship was assessed during transient reduction of CPP from 100 to 30 mmHg. Coronary hyperemic flow due to adenosine and papaverine was attenuated 30 min after transient 10- and 15-min periods of ischemia. In the group of transient 10-min ischemia, both fractional shortening (FS) and CBF returned to the preischemic values at 30 and 60 min of reperfusion; however, marked decreases in CBF (35 +/- 5 vs. 56 +/- 4 ml.100 g-1.min-1 at CPP = 60 mmHg, P < 0.01) during graded reductions in CPP were observed. The endomyocardial blood flow was reduced relative to the control condition. Furthermore, both FS (6 +/- 1 vs. 14 +/- 1% at CPP = 60 mmHg, P < 0.01) and lactate extraction ratio (-41 +/- 15 vs. 1 +/- 6% at CPP = 60 mmHg, P < 0.05) were decreased. The downward shift of the CPP-CBF relationship and the deterioration of myocardial contractile and metabolic function during reduction of CPP were restored 60 min after the onset of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Selective large coronary endothelial dysfunction in conscious dogs with chronic coronary pressure overload

1998 ◽  
Vol 274 (2) ◽  
pp. H539-H551 ◽  
Author(s):  
Bijan Ghaleh ◽  
Luc Hittinger ◽  
Song-Jung Kim ◽  
Raymond K. Kudej ◽  
Mitsunori Iwase ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Coronary Arteries ◽  
Perfusion Pressure ◽  
Pressure Overload ◽  
Coronary Perfusion Pressure ◽  
Conscious Dogs ◽  
Systemic Hypertension ◽  
Coronary Perfusion ◽  
Coronary Pressure ◽  
Large Coronary Arteries

Coronary vascular responses to acetylcholine (ACh, 3 μg/kg iv), nitroglycerin (NTG, 25 μg/kg iv), and a 20-s coronary artery occlusion (reactive hyperemia, RH) were investigated in seven conscious dogs with severe left ventricular (LV) hypertrophy and chronic coronary pressure overload (CCPO) due to supravalvular aortic banding and in seven control dogs. All dogs were instrumented for measurement of ultrasonic coronary diameter (CD) and Doppler coronary blood flow (CBF). LV-to-body weight ratio was increased by 82% in CCPO dogs. In control dogs, ACh increased CD (+5.9 ± 1.7%). This response was reduced ( P < 0.05) in CCPO dogs (+1.9 ± 0.9%). Similarly, flow-mediated increases in CD after RH were blunted ( P < 0.01) in CCPO (+2.1 ± 0.8) vs. control dogs (+6.8 ± 1.8%). In contrast, ACh and RH increased CBF similarly in both groups. Increases in both CD and CBF to NTG were not different between control dogs and CCPO. Peak systolic CBF velocity was greater, P< 0.01, in CCPO (94 ± 17 cm/s) compared with control (35 ± 7 cm/s) dogs, most likely secondary to the increased systolic coronary perfusion pressure (215 vs. 130 mmHg). Histological analyses of large coronary arteries in CCPO revealed medial thickening, intimal thickening, and disruption of the internal elastic lamina and endothelium. In contrast, small intramyocardial arterioles failed to show the intimal and endothelial lesions. Thus, in CCPO selective to the coronary arteries, i.e., a model independent from systemic hypertension and enhanced levels of plasma renin activity, endothelial control was impaired for both flow-mediated and receptor-mediated large coronary artery function, which could be accounted for by the major morphological changes in the large coronary arteries sparing the resistance vessels. The mechanism may involve chronically elevated systolic coronary perfusion pressure, CBF velocity, and potential disruption of laminar flow patterns.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

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