LV pressure-volume area and oxygen consumption: evaluation in intact dog by fast CT

1990 ◽  
Vol 258 (4) ◽  
pp. H1208-H1215
Author(s):  
N. Chung ◽  
X. Wu ◽  
K. R. Bailey ◽  
E. L. Ritman
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Ct Scanner ◽  
Beta Adrenergic ◽  
The Relationship

The relationship between left ventricular (LV) myocardial oxygen consumption (MVO2) and LV systolic pressure-volume area (PVA) was investigated in anesthetized closed-chest dogs with intact reflexes and subsequently with beta-adrenergic blockade, with or without simultaneous muscarinic blockade. LV chamber volumes were measured using a fast computerized tomography (CT) scanner (dynamic spatial reconstructor, DSR) at 33-ms intervals. Myocardial blood flow was measured from the DSR scans of aortic root angiograms. With intact reflexes, LV MVO2 (Y) related to PVA (X) values as Y = (4.28 +/- 1.81)X + (1.94 +/- 6.0) (n = 24) (mJ.g-1.cycle-1). With beta-adrenergic blockade, LV MVO2 (Y) related to PVA (X) value as Y = (4.24 +/- 1.03)X - (6.43 +/- 6.5), (n = 9) (mJ.g-1.cycle-1). With beta-adrenergic and muscarinic blockade, LV MVO2 (Y) related to PVA (X) value as Y = (2.84 +/- 1.72)X + (3.51 +/- 5.15), (n = 13) (mJ.g-1.cycle-1). The slopes of these regressions are higher than the slopes demonstrated by others in isolated ventricles but very similar to those demonstrated in open-chest dogs.

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.

Left ventricular oxygen consumption and function in hypoxemia in conscious lambs

1983 ◽  
Vol 244 (5) ◽  
pp. H664-H671 ◽  
Author(s):  
D. J. Fisher
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Oxygen Content ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Blood Oxygen ◽  
Aortic Blood ◽  
Coronary Sinus Blood

The effects of hypoxemia on left ventricular myocardial blood flow, myocardial oxygen consumption, and contractile function were studied in 12 conscious newborn lambs 4-24 days after birth. Through a left thoracotomy, we placed fluid-filled catheters in the ascending aorta, coronary sinus, and left atrium. An electromagnetic flow transducer was placed around the ascending aorta, and a solid-state pressure transducer was introduced into the left ventricle. Three to four days later we measured aortic and coronary sinus blood oxygen contents, left ventricular myocardial blood flow, heart rate, aortic and left ventricular blood pressures, ascending aortic blood flow velocity, and the first derivative of left ventricular pressure (dP/dt) and ascending aortic blood flow velocity (dV/dt) during a control period and during 50 and 75% reductions in ascending aortic oxygen content. Myocardial oxygen consumption was calculated. There was no significant change in aortic or coronary sinus blood pH or CO2 tension during the study. Coronary sinus blood oxygen content and the arteriovenous difference of oxygen across the left ventricle decreased as a linear function of the aortic blood oxygen content. Myocardial blood flow increased in proportion to the reduction in aortic blood oxygen content. Myocardial oxygen consumption increased during hypoxemia but not as a function of aortic blood oxygen content. There was no significant change in left ventricular end-diastolic pressure or aortic mean blood pressure. dP/dt and dV/dt doubled during hypoxemia, but the increases did not occur as a function of the aortic blood oxygen content. In conscious, unanesthetized newborn lambs, 50 and 75% reductions of aortic blood oxygen content were associated with significant increases of left ventricular myocardial blood flow, oxygen consumption, and contractile function.

Myocardial energetics and blood flow in acute rapid ventricular pacing

1994 ◽  
Vol 72 (1) ◽  
pp. 6-10 ◽  
Author(s):  
William W. Simmons ◽  
Gordon W. Moe ◽  
Etienne A. Grima ◽  
Robert J. Howard ◽  
Paul W. Armstrong
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Adenine Nucleotide ◽  
Severe Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Pacing ◽  
Hemodynamic Deterioration ◽  
Rapid Ventricular Pacing

The mechanism whereby chronic rapid ventricular pacing induces severe heart failure is unclear, but the phenomenon is associated with a reduction in left ventricular ATP levels. Accordingly, the current study was undertaken to evaluate the acute effects of rapid ventricular pacing on hemodynamics, left ventricular adenine nucleotide levels, myocardial blood flow, and oxygen consumption. Anesthetized dogs (n = 7) were studied in sinus rhythm and during 30 min of pacing at 250 beats/min. Pacing caused a significant (means ± SD, all p < 0.001) decrease in cardiac output (3.0 ± 0.6 to 2.0 ± 0.6 L/min) and peak left ventricular systolic pressure (133 ± 14 to 82 ± 10 mmHg (1 mmHg = 133.3 Pa)) and an increase in pulmonary wedge pressure (10 ± 2 to 18 ± 3 mmHg). Following pacing, the peak first derivative of left ventricular pressure and the relaxation time constant, τ, remained unchanged compared with baseline values. Myocardial blood flow and oxygen consumption both increased by 70% with pacing. The transmural distribution of myocardial blood flow and myocardial lactate consumption remained unchanged. There was no change in left ventricular ATP or ADP levels with the observed increase in myocardial oxygen consumption. Therefore, the hemodynamic deterioration associated with acute rapid ventricular pacing, in contrast to that of chronic pacing, is not associated with perturbed myocardial energetics.Key words: canine, ventricular pacing, ATP, ADP, myocardial blood flow, ventricular function.

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Oxygen Delivery ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

Coronary hyperperfusion augments myocardial oxygen consumption

1996 ◽  
Vol 271 (4) ◽  
pp. H1384-H1393 ◽  
Author(s):  
Y. Ishibashi ◽  
J. Zhang ◽  
D. J. Duncker ◽  
C. Klassen ◽  
T. Pavek ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Contractile Function ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Systolic Thickening ◽  
Subepicardial Layer ◽  
Systolic Wall Thickening

This study was performed to test the hypothesis that increases in myocardial oxygen consumption (MVo2) and myocardial contractile function during exercise are flow limited. Studies were performed in 15 chronically instrumented normal dogs. MVo2 and regional percent systolic wall thickening were measured during control conditions and during maximal vasodilation produced by infusion of adenosine (20-75 micrograms.kg-1.min-1) or adenosine combined with nitroglycerin (0.4 micrograms.kg-1.min-1; TNG) into the left anterior descending coronary artery during a three-stage graded treadmill exercise protocol. Adenosine and adenosine plus TNG significantly increased coronary blood flow by 298 +/- 26 and 306 +/- 24%, respectively, at rest and by 134 +/- 7 and 145 +/- 9%, respectively, during the heaviest level of exercise (each P < 0.01). Adenosine and adenosine plus TNG increased MVo2 at rest, but this was associated with a parallel increase in heart rate, so that MVo2 per beat was not significantly changed. Systolic wall thickening was also not changed by hyperperfusion during resting conditions. However, MVo2 per beat was increased by 12 +/- 4% with adenosine and by 13 +/- 5% with adenosine plus TNG during moderate exercise and by 23 +/- 5% with adenosine and by 27 +/- 4% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). Systolic thickening of the full left ventricular wall did not change during hyperperfusion, but thickening in the subepicardial layer was increased by 14 +/- 3% with adenosine and 18 +/- 3% with adenosine plus TNG during the heaviest level of exercise (each P < 0.05). There was no difference in wall thickening between adenosine and adenosine plus TNG. These findings imply that the increases in MVo2 which occur during exercise are limited by coronary blood flow.

The relationship between myocardial oxygen consumption and total work obtained by a new left ventricular model

1984 ◽  
Vol 79 (3) ◽  
pp. 363-374
Author(s):  
Sh. Satoh ◽  
Y. Shimizu ◽  
Y. Maruyama ◽  
K. Ashikawa ◽  
Sh. Isoyama ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
New Left ◽  
Left Ventricular ◽  
Total Work ◽  
The Relationship

Comparative effects of levosimendan, OR-1896, OR-1855, dobutamine, and milrinone on vascular resistance, indexes of cardiac function, and O2 consumption in dogs

2008 ◽  
Vol 294 (1) ◽  
pp. H238-H248 ◽  
Author(s):  
Patricia N. Banfor ◽  
Lee C. Preusser ◽  
Thomas J. Campbell ◽  
Kennan C. Marsh ◽  
James S. Polakowski ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulse Pressure ◽  
Myocardial Oxygen Consumption ◽  
Plasma Concentrations ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Dose Dependent

Levosimendan enhances cardiac contractility via Ca2+ sensitization and induces vasodilation through the activation of ATP-dependent K+ and large-conductance Ca2+-dependent K+ channels. However, the hemodynamic effects of levosimendan, as well as its metabolites, OR-1896 and OR-1855, relative to plasma concentrations achieved, are not well defined. Thus levosimendan, OR-1896, OR-1855, or vehicle was infused at 0.01, 0.03, 0.1, and 0.3 μmol·kg−1·30 min−1, targeting therapeutic to supratherapeutic concentrations of total levosimendan (62.6 ng/ml). Results were compared with those of the β1-agonist dobutamine and the phosphodiesterase 3 inhibitor milrinone. Peak concentrations of levosimendan, OR-1896, and OR-1855 were 455 ± 21, 126 ± 6, and 136 ± 6 ng/ml, respectively. Levosimendan and OR-1896 produced dose-dependent reductions in mean arterial pressure (−31 ± 2 and −42 ± 3 mmHg, respectively) and systemic resistance without affecting pulse pressure, effects paralleled by increases in heart rate; OR-1855 produced no effect at any dose tested. Dobutamine, but not milrinone, increased mean arterial pressure and pulse pressure (17 ± 2 and 23 ± 2 mmHg, respectively). Regarding potency to elicit reductions in time to peak pressure and time to systolic pressure recovery: OR-1896 > levosimendan > milrinone > dobutamine. Levosimendan and OR-1896 elicited dose-dependent increases in change in pressure over time (118 ± 10 and 133 ± 13%, respectively), concomitant with reductions in left ventricular end-diastolic pressure and ejection time. However, neither levosimendan nor OR-1896 produced increases in myocardial oxygen consumption at inotropic and vasodilatory concentrations, whereas dobutamine increased myocardial oxygen consumption (79% above baseline). Effects of the levosimendan and OR-1896 were limited to the systemic circulation; neither compound produced changes in pulmonary pressure, whereas dobutamine produced profound increases (74 ± 13%). Thus levosimendan and OR-1896 are hemodynamically active in the anesthetized dog at concentrations observed clinically and elicit cardiovascular effects consistent with activation of both K+ channels and Ca2+ sensitization, whereas OR-1855 is inactive on endpoints measured in this study.

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