scholarly journals Myocardial ischemia: lack of coronary blood flow, myocardial oxygen supply-demand imbalance, or what?

2019 ◽  
Vol 316 (6) ◽  
pp. H1439-H1446 ◽  
Author(s):  
Gerd Heusch
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Oxygen Supply ◽  
Contractile Function ◽  
Historical Background ◽  
Prevailing Paradigm ◽  
And Function ◽  
Myocardial Oxygen Supply

This opinionated article reviews current concepts of myocardial ischemia. Specifically, the historical background is briefly presented. Then, the prevailing paradigm of myocardial oxygen-supply-demand imbalance is criticized since demand is a virtual parameter that cannot be measured and data on measurements of myocardial blood flow and contractile function rather support matching between flow and function. Finally, a concept of myocardial ischemia that focusses on the reduction of coronary blood flow to below 8–10 µl/g per beat with consequences for myocardial electrical, metabolic, contractile and morphological features is advocated.

Role of cardiac mast cells in complement C5a-induced myocardial ischemia

1993 ◽  
Vol 264 (5) ◽  
pp. H1346-H1354 ◽  
Author(s):  
B. R. Ito ◽  
R. L. Engler ◽  
U. del Balzo
Keyword(s):  
Blood Flow ◽  
Mast Cell ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow ◽  
Cell Activation ◽  
Mast Cell Degranulation ◽  
Mast Cell Activation ◽  
Coronary Vein ◽  
Arterial Blood ◽  
Complement C5a

Activated complement component C5a causes myocardial ischemia mediated by thromboxane (Tx) A2 and leukotrienes C4/D4. Blood cells are not involved in either the mediator release or the myocardial effects of C5a, suggesting that a C5a-sensitive, cardiac resident inflammatory cell is responsible. The goals of this study were to determine whether 1) cardiac mast cell activation accompanies the C5a response, 2) inhibition of mast cell degranulation inhibits the response, and 3) histamine release plays a role in the C5a-induced myocardial ischemia. The left anterior descending coronary artery (LAD) of open-chest pigs (n = 13) was perfused with arterial blood at constant pressure (95 mmHg). Coronary blood flow (CBF) was measured (in-line flowmeter) and regional function [percent segment shortening (%SS)] determined with sonomicrometry. A coronary vein was cannulated for measurement of plasma TxB2 and histamine (a marker of mast cell degranulation). Intracoronary C5a (500 ng) decreased coronary blood flow (45% of preinfusion levels) and LAD %SS (65% of preinfusion) and was accompanied by increases in coronary venous TxB2 (delta 63.3 ng/ml) and histamine (delta 200 nM). Mast cell inhibition with lodoxamide (2 mg/kg iv, n = 8) attenuated the C5a-induced fall in CBF (14 vs. 53% decrease, P < 0.01) and %SS (10 vs. 38% decrease, P < 0.01) and also reduced the C5a-induced increase in both coronary venous histamine (delta 26 vs. 278 nM, P < 0.05) and TxB2 (delta 0.34 vs. 63.3 ng/ml, P < 0.01). However, histamine H1 (pyrilamine) and H2 (ranitidine) receptor blockade had no effect on the C5a-induced fall in CBF or LAD %SS.(ABSTRACT TRUNCATED AT 250 WORDS)

Alteration in myocardial oxygen balance during exercise after beta-adrenergic blockade in dogs

1980 ◽  
Vol 49 (1) ◽  
pp. 28-33 ◽  
Author(s):  
G. R. Heyndrickx ◽  
J. L. Pannier ◽  
P. Muylaert ◽  
C. Mabilde ◽  
I. Leusen
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Oxygen Balance

The effects of beta-adrenergic blockade upon myocardial blood flow and oxygen balance during exercise were evaluated in eight conscious dogs, instrumented for chronic measurements of coronary blood flow, left ventricular pressure, aortic blood pressure, heart rate, and sampling of arterial and coronary sinus venous blood. The administration of propranolol (1.5 mg/kg iv) produced a decrease in heart rate, peak left ventricular (LV) dP/dt, LV (dP/dt/P, and an increase in LV end-diastolic pressure during exercise. Mean coronary blood flow and myocardial oxygen consumption were lower after propranolol than at the same exercise intensity in control conditions. The oxygen delivery-to-oxygen consumption ratio and the coronary sinus oxygen content were also significantly lower. It is concluded that the relationship between myocardial oxygen supply and demand is modified during exercise after propranolol, so that a given level of myocardial oxygen consumption is achieved with a proportionally lower myocardial blood flow and a higher oxygen extraction.

Myocardial blood flow and coronary reserve in chronically anemic fetal lambs

1999 ◽  
Vol 277 (1) ◽  
pp. R306-R313 ◽  
Author(s):  
Lowell E. Davis ◽  
A. Roger Hohimer ◽  
Mark J. Morton
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Adenosine Infusion ◽  
Fetal Sheep ◽  
Coronary Reserve ◽  
Flow Reserve ◽  
Coronary Conductance ◽  
The Difference

Chronic fetal anemia produces large compensatory increases in coronary blood flow in the near-term fetal lamb. To determine if increased coronary flow in anemic fetuses is associated with decreased coronary flow reserve or, alternatively, an increase in coronary conductance, we measured maximal coronary artery conductance during adenosine infusion before and during anemia. Isovolemic hemorrhage over 7 days reduced hematocrit from 30.6 ± 2.7 to 15.8 ± 2.4% ( P < 0.02) and the oxygen content from 7.3 ± 1.4 to 2.6 ± 0.4 ml/dl ( P < 0.001). Coronary blood flow increased from control (202 ± 60) to 664 ± 208 ml ⋅ min−1 ⋅ 100 g−1 with adenosine to 726 ± 169 ml ⋅ min−1 ⋅ 100 g−1 during anemia and to 1,162 ± 250 ml ⋅ min−1 ⋅ 100 g−1 (left ventricle) during anemia with adenosine infusion (all P< 0.001). Coronary conductance, determined during maximal vasodilation, was 18.2 ± 7.7 before and 32.8 ± 11.9 ml ⋅ min−1 ⋅ 100 g−1 ⋅ mmHg−1during anemia ( P < 0.001). Coronary reserve, the difference between resting and maximal myocardial blood flow interpolated at 40 mmHg, was unchanged in control and anemic fetuses (368 ± 142 and 372 ± 201 ml/min). Because hematocrit affects viscosity, anemic fetuses were transfused with blood to acutely increase the hematocrit back to control, and conductance was remeasured. Coronary blood flow decreased 57.3 ± 18.9% but was still 42.6 ± 18.9% greater than control. We conclude that in chronically anemic fetal sheep coronary conductance is increased and coronary reserve is maintained, and this is attributed in part to angiogenesis as well as changes in viscosity.

Coronary Blood Flow and Myocardial Ischemia

2007 ◽  
pp. 439-449
Author(s):  
Robert J. Henning ◽  
Ray A. Olsson
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow

Myocardial blood flow and function with critical coronary stenosis in exercising dogs

1982 ◽  
Vol 243 (5) ◽  
pp. H698-H707 ◽  
Author(s):  
K. P. Gallagher ◽  
G. Osakada ◽  
M. Matsuzaki ◽  
W. S. Kemper ◽  
J. Ross
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Wall Thickening ◽  
Critical Stenosis ◽  
Vasodilator Reserve ◽  
Primary Determinant ◽  
And Function ◽  
Systolic Wall Thickening ◽  
Coronary Blood Flow Velocity ◽  
Contractile Performance

Critical stenosis of coronary arteries does not alter myocardial blood flow (MBF) at rest, but eliminates hyperemia and corresponds to a degree of arterial narrowing that expends subendocardial vasodilator reserve. Because subepicardial vasodilator reserve remains with critical stenosis at rest, we tested the significance of this reserve in six exercising dogs chronically instrumented to measure MBF (microspheres), regional function (systolic wall thickening with sonomicrometers), and coronary blood flow velocity (CBFV, pulsed Doppler). Critical stenosis produced with a hydraulic occluder limited CBFV and mean MBF to the resting level during treadmill exercise, but MBF was maldistributed. Subendocardial MBF decreased 50% (P less than 0.05) and subepicardial MBF increased 104% (P less than 0.01) compared with resting control conditions, suggesting that a transmural "steal" phenomenon had occurred, with augmented MBF in the subepicardial region at the expense of subendocardial MBF. Systolic wall thickening decreased markedly from 31.5 +/- 6.8 to 9.4 +/- 2.0% (P less than 0.01) during exercise, indicating that use of subepicardial vasodilator reserve with critical stenosis had little sustaining effect on regional contractile performance. Rather, subepicardial vasodilator reserve is potentially deleterious, inasmuch as a steal effect could contribute to reduced subendocardial perfusion, the primary determinant of systolic wall thickening.

Heterogeneity of myocardial blood flow under normal conditions and its dependence on arterial PO2

1990 ◽  
Vol 258 (2) ◽  
pp. H549-H555 ◽  
Author(s):  
H. G. Wolpers ◽  
A. Hoeft ◽  
H. Korb ◽  
P. R. Lichtlen ◽  
G. Hellige
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Arterial Oxygen Tension ◽  
Inert Gases ◽  
Arterial Oxygen ◽  
Tracer Gas ◽  
Stochastic Description ◽  
Flow Reserve ◽  
Arterial Po2

We studied the heterogeneity of myocardial blood flow in nine anesthetized closed-chest dogs using an indicator-dilution technique that allows the stochastic description of transport characteristics for three inert gases (helium, argon, and xenon) from the coronary inflow to outflow. The results show that under normal conditions the transcoronary transport of the tracers is spatially heterogeneous. Heterogeneity is strongly dependent on the arterial oxygen tension over a range of 40–200 Torr. This could be similarly observed with each tracer gas despite different physicochemical properties and was largely independent from the magnitude of coronary blood flow. The results are interpreted to mean that the arteriolar or intratissue PO2 influences myocardial blood flow over a broad range and possibly acts as an important integrating factor in the local regulation of coronary blood flow and flow reserve.

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