Effect of Catecholamines, l-Epinephrine and l-Norepinephrine on Coronary Flow and Oxygen Metabolism of the Myocardium

1958 ◽  
Vol 193 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Harold Feinberg ◽  
Louis N. Katz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Coronary Flow ◽  
Myocardial Oxygen Consumption ◽  
Oxygen Metabolism ◽  
Aortic Pressure ◽  
Coronary Vasodilatation ◽  
Oxygen Difference ◽  
Mean Aortic Pressure

The effect of continuously infused intravenous l-epinephrine and l-norepinephrine (0.1–2.5 gamma/kg/min.) was determined in the open-chest, anesthetized dog prepared for measurement of total coronary flow. Coronary blood flow, myocardial oxygen availability and coronary venous oxygen content consistently increased after catecholamine administration despite wide fluctuations, above and below control values, in heart rate and mean aortic pressure at constant cardiac output. Thus, there was a significant decrease in the coronary arteriovenous oxygen difference after catecholamine administration. The increase in coronary flow and decrease in the coronary A-V oxygen difference were seen even when blood pressure and heart rate were lowered. It is concluded that the departure from the usual relationship between coronary flow and myocardial oxygen consumption is attributable to coronary vasodilatation. However, myocardial oxygen consumption is still the primary factor controlling coronary flow during catecholamine action.

Myocardial oxygen consumption and coronary blood flow in hypothermia

1959 ◽  
Vol 196 (4) ◽  
pp. 719-725 ◽  
Author(s):  
A. Gerola ◽  
H. Feinberg ◽  
L. N. Katz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Coronary Flow ◽  
Myocardial Oxygen Consumption ◽  
Control Period ◽  
Mechanical Efficiency ◽  
Individual Variability ◽  
Large Individual ◽  
Oxygen Requirement

Effects of hypothermia (at 32° and 27°C) were determined in the open-chest anesthetized dog prepared for measurement of total coronary flow and myocardial oxygen consumption. When hypothermia was induced at any fixed cardiac output, cardiac oxygen consumption and heart rate declined while blood pressure remained constant. Cardiac external mechanical efficiency increased at the same time. Hypothermia did not alter the relationship between the myocardial oxygen requirement and the total cardiac effort as indicated by the product of blood pressure times heart rate. Without regard to the large individual variability, the coronary venous O2 rose; thus the general trend during the induction of hypothermia was a decline in the coronary A-V oxygen difference, the percentage O2 extracted by the heart and the ratio: cardiac O2 consumption/O2 availability. The coronary venous O2 content and the coronary A-V O2 difference remained fairly constant as the cardiac effort and its oxygen requirement varied during hypothermia, just as in the control period. Thus coronary flow was the only means of adjusting to the altered cardiac oxygen need in both periods.

Role of catecholamines on energetics of the heart and its blood supply

1959 ◽  
Vol 196 (2) ◽  
pp. 394-400 ◽  
Author(s):  
A. Gerola ◽  
H. Feinberg ◽  
L. N. Katz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Coronary Flow ◽  
Direct Action ◽  
Coronary Vessels ◽  
Mechanical Efficiency ◽  
Oxygen Requirement ◽  
Oxygen Difference

The effects of continuously infused intravenous l-epinephrine and l-norepinephrine (5 gamma/ kg/min.) were determined in the open-chested anesthetized dog prepared for measurement of total coronary flow and myocardial oxygen consumption. When catecholamines were infused at any fixed cardiac output, cardiac oxygen consumption rose in association with increases in blood pressure and heart rate, while cardiac external mechanical efficiency declined. The significance of the product (blood pressure times heart rate) as an index of the total cardiac effort, as indicated by the myocardial oxygen requirement, is considered in view of the alterations brought about by catecholamines in this relationship. The decline in the coronary A-V oxygen difference, the percentage of oxygen extracted by the heart and the ratio (cardiac oxygen consumption/oxygen availability) and the rise in coronary venous oxygen, are all attributed to a direct action of catecholamines on the coronary vessels. Despite their new levels, the coronary venous oxygen, content and the coronary A-V oxygen difference remain fairly constant as the cardiac effort and its oxygen requirement vary during catecholamine infusion.

Effect of changes in blood CO2 level on coronary flow and myocardial O2 consumption

1960 ◽  
Vol 199 (2) ◽  
pp. 349-354 ◽  
Author(s):  
H. Feinberg ◽  
A. Gerola ◽  
L. N. Katz
Keyword(s):  
Oxygen Consumption ◽  
Coronary Flow ◽  
Myocardial Oxygen Consumption ◽  
Gas Mixture ◽  
Aortic Blood ◽  
Anesthetized Dogs ◽  
Myocardial O2 Consumption ◽  
Aortic Blood Pressure ◽  
Co2 Level ◽  
Oxygen Difference

The effect of hypo- and hypercapnia—induced by changing the respiratory gas mixture—on coronary flow and myocardial oxygen consumption was observed at constant cardiac output and over a broad range of pressure-loads in open-chested, anesthetized dogs. The correlation of cardiac effort (as indexed by the product of heart rate and mean aortic blood pressure) with myocardial oxygen consumption was not altered by increasing or decreasing the arterial CO2 content. Coronary blood flow was observed to be increased relative to the cardiac effort during hypercapnia but not during hypocapnia. The coronary arteriovenous oxygen difference and the percentage of oxygen extracted decreased during hypercapnia pari passu with the increase in venous oxygen content.

Effect of excitement on coronary and systemic energetics in unanesthetized dogs

1965 ◽  
Vol 209 (4) ◽  
pp. 680-688 ◽  
Author(s):  
Claudia R. Rayford ◽  
Edward M. Khouri ◽  
Donald E. Gregg
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Coronary Flow ◽  
Cardiac Cycle ◽  
Myocardial Metabolism ◽  
Aortic Pressure ◽  
Moderate Increase ◽  
Sizeable Increase

The effect of excitement on phasic aortic pressure and flow, phasic left coronary flow, and myocardial metabolism has been studied in dogs 1–8 weeks after implantation of appropriate flowmeters and other devices. The rapid increase in heart rate and mild increase in blood pressure in the first few seconds tend to maintain coronary flow per minute despite a decrease in stroke cardiac output and coronary flow throughout the cardiac cycle. The main response is a delayed rise in coronary flow per minute resulting from further elevation of heart rate and blood pressure, a moderate increase in stroke cardiac output and a sizeable increase in stroke coronary flow, the latter being divided fairly evenly between systole and diastole. From 60 to 90% of the increase in mean coronary flow arises from the increase in stroke coronary flow, and the remainder from the increased number of heartbeats per minute. Some of the possible mechanisms concerned are discussed.

Blockade of beta-adrenoceptor in control of blood pressure in fowl

1995 ◽  
Vol 269 (4) ◽  
pp. R914-R922 ◽  
Author(s):  
K. Kamimura ◽  
H. Nishimura ◽  
J. R. Bailey
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Aortic Pressure ◽  
Induced Hypotension ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Mean Aortic Pressure ◽  
Beta Adrenoceptor Blockers

Several avian species show elevated blood pressure (BP) and spontaneous atherogenesis in the aorta and other large arteries. The BP appears to be influenced by age, sex (higher in males), environment, and diet in some species. We reported previously that mean aortic pressure and heart rate, but not plasma renin activity (PRA), of conscious female domestic fowl were markedly reduced by propranolol. In the present study, we aimed to determine in conscious roosters whether 1) hypotension evoked by atenolol or practolol, which selectively inhibit cardiac beta-receptors in mammals, is more potent than that evoked by propranolol, and 2) the renin-angiotensin (ANG) system and/or catecholamines are involved in beta-adrenoceptor antagonist-induced hypotension. Mean arterial pressure (171.2 +/- 3.5 mmHg) and heart rate (281 +/- 4 beats/min) of chronically cannulated roosters (n = 38) were markedly reduced by acute infusion or repeated injections (14 days) of propranolol, atenolol, or practolol, but not by SQ-14,225 (ANG-converting enzyme inhibitor) or [Sar1, Thr8]ANG II (nonselective ANG receptor antagonist). None of the beta-adrenoceptor blockers, however, showed cardioselectivity. The resting PRA of conscious roosters (1.27 +/- 0.09 ng.ml-1.h-1, n = 38) was low and did not change significantly after chronic or acute treatment with beta-adrenoceptor blockers except for a slight decrease induced by practolol. PRA increased after SQ-14,225. The plasma levels (pg/ml) of norepinephrine (701.9 +/- 76.0), epinephrine (337.2 +/- 57.1), and dopamine (299.1 +/- 39.0) of conscious roosters were further increased by propranolol. Practolol also increased dopamine significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial Oxygen Consumption Index in Patients with Coronary Artery Disease

2005 ◽  
Vol 13 (1) ◽  
pp. 34-37 ◽  
Author(s):  
Arash Arya ◽  
Majid Maleki ◽  
Fereydoon Noohi ◽  
Ebrahim Kassaian ◽  
Farideh Roshanali
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Coronary Artery ◽  
Myocardial Oxygen Consumption ◽  
Activity Level ◽  
Home Based ◽  
Consumption Index ◽  
Artery Disease

One hundred and thirty-six men with coronary artery disease were randomly assigned to a hospital-based or home-based exercise program of 3 sessions per week. A treadmill test was carried out with the modified Naughton protocol. After 3 months, 125 patients (92%) with a mean age of 55 ± 11 years had completed the study. Maximum workload achieved increased by 65% [(12.40 ± 1.32 vs. 7.50 ± 0.85 metabolic equivalent units (METs)] in the hospital-based group, and by 17% (8.86 ± 0.9 vs. 7.56 ± 0.78 METs) in the home-based group ( p = 0.0001). The heart rate-blood pressure product, an index of myocardial oxygen consumption, decreased at rest by 19% in the hospital-based group but was unchanged in the home-based group ( p = 0.0001). The heart rate-blood pressure product at 5 and 7 METs activity level decreased 28% and 26%, respectively, in the hospital-based group vs. 8% and 2% in the home-based group ( p = 0.0001). It was concluded that hospital-based exercise training in patients with coronary artery disease improves functional capacity and decreases the myocardial oxygen consumption index at rest and during exercise.

Effects of Heart Rate on Coronary Flow and Cardiac Oxygen Consumption

1956 ◽  
Vol 185 (2) ◽  
pp. 355-364 ◽  
Author(s):  
D. Laurent ◽  
C. Bolene-Williams ◽  
F. L. Williams ◽  
L. N. Katz
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Coronary Flow ◽  
High Energy ◽  
Cardiac Work ◽  
Spontaneous Change ◽  
Ordinary Type ◽  
Relationship Of ◽  
The Relationship ◽  
Oxygen Difference

The effects of electrically-induced heart rate (up to 300 beats/min.) on coronary flow and cardiac oxygen consumption has been studied in an open-chested intact preparation. A significant correlation between heart rate, coronary flow and cardiac oxygen consumption has been found at each level of cardiac work. Coronary flow and cardiac oxygen consumption increase with a rise in heart rate and seem to approach a limit at extremely rapid heart rates. Nomograms relating heart rate, work and oxygen consumption of the heart have been constructed. From these it is seen that heart rate is an important factor in determining the myocardial oxygen consumption; this is true at each level of cardiac work. The significance of these findings have been discussed relative to the unanesthetized animal. Under conditions of excessive heart rate or cardiac load which presumably lead to unusually high energy requirements, a radical departure from the expected ‘normal’ values was found in coronary flow, coronary A-V oxygen difference and cardiac oxygen consumption. This confirms the presence of ‘spontaneous’ change previously described by us. Its meaning and significance is discussed. Under these conditions of ‘spontaneous’ change coronary flow was increased, oxygen consumption decreased and coronary venous oxygen was raised as the coronary A-V oxygen difference declined. This ‘spontaneous’ change shifted the relationship of coronary flow to oxygen consumption. Furthermore, it led to a rise in coronary flow despite an elevation in coronary venous oxygen. It would seem that at this time the energy metabolism of the heart must change in that less oxygen is extracted from the blood despite an increase in its availability. The heart may therefore operate anaerobically in part or may make use of other hydrogen acceptors in the blood. The fact that this kind of metabolism may last as long as an hour or more, excludes the ordinary type of ‘oxygen debt.’

Adenosine is not responsible for local metabolic control of coronary blood flow in dogs during exercise

2000 ◽  
Vol 278 (1) ◽  
pp. H74-H84 ◽  
Author(s):  
Johnathan D. Tune ◽  
Keith Neu Richmond ◽  
Mark W. Gorman ◽  
Ray A. Olsson ◽  
Eric O. Feigl
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Metabolic Control ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Aortic Pressure ◽  
Receptor Blockade ◽  
Adenosine Concentration ◽  
Venous Plasma

The purpose of this investigation was to quantitatively evaluate the role of adenosine in coronary exercise hyperemia. Dogs ( n = 10) were chronically instrumented with catheters in the aorta and coronary sinus, and a flow probe on the circumflex coronary artery. Cardiac interstitial adenosine concentration was estimated from arterial and coronary venous plasma concentrations using a previously tested mathematical model. Coronary blood flow, myocardial oxygen consumption, heart rate, and aortic pressure were measured at rest and during graded treadmill exercise with and without adenosine receptor blockade with either 8-phenyltheophylline (8-PT) or 8- p-sulfophenyltheophylline (8-PST). In control vehicle dogs, exercise increased myocardial oxygen consumption 4.2-fold, coronary blood flow 3.8-fold, and heart rate 2.5-fold, whereas mean aortic pressure was unchanged. Coronary venous plasma adenosine concentration was little changed with exercise, and the estimated interstitial adenosine concentration remained well below the threshold for coronary vasodilation. Adenosine receptor blockade did not significantly alter myocardial oxygen consumption or coronary blood flow at rest or during exercise. Coronary venous and estimated interstitial adenosine concentration did not increase to overcome the receptor blockade with either 8-PT or 8-PST as would be predicted if adenosine were part of a high-gain, negative-feedback, local metabolic control mechanism. These results demonstrate that adenosine is not responsible for local metabolic control of coronary blood flow in dogs during exercise.

Cardiovascular response to graded exercise in the sympathectomized-vagotomized dog

1963 ◽  
Vol 204 (2) ◽  
pp. 291-296 ◽  
Author(s):  
Edmundo Ashkar ◽  
William F. Hamilton
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Stroke Volume ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Graded Exercise ◽  
Oxygen Difference

Seven dogs who ran well on a motor-driven treadmill were completely sympathectomized (including adrenal denervation) and subjected to unilateral vagotomy below the recurrent laryngeal branch. After recovery and retraining, a terminal experiment was performed in which, after completing the vagotomy, direct Fick determinations of cardiac output and continuous recordings of mean arterial pressure, heart rate, and oxygen consumption were made at rest and during increasing exercise The results were compared with those described by Barger et al. ( Am. J. Physiol. 184: 613, 1956) for normal dogs running at smaller speeds and grades. The heart rate of the operated dogs increased from 117 to 134. Barger's normal dogs doubled their heart rate. The A-V oxygen difference increased with work slightly less than Barger's normal dogs but the scatter in both groups was wide, as was the case with the stroke volume. The resting cardiac output was nearly normal in the operated dogs but increased only 34% with exercise, as against 200–300% in Barger's normals. Oxygen consumption increased about twofold as against the expected normal of three- to sevenfold. Peripheral resistance in both groups went down about 40%. The blood pressure in the normal increased substantially while that in the operated dogs fell about 20% to an average of 60 mm Hg.

Determinants of coronary flow and myocardial oxygen consumption

1962 ◽  
Vol 202 (1) ◽  
pp. 45-52 ◽  
Author(s):  
H. Feinberg ◽  
L. N. Katz ◽  
E. Boyd
Keyword(s):  
Coronary Flow ◽  
Myocardial Oxygen Consumption ◽  
Vascular Tone ◽  
Aortic Pressure ◽  
Energy Utilization ◽  
Hemodynamic Parameters ◽  
Coronary Vascular Tone ◽  
Myocardial Oxygen Extraction ◽  
High Level ◽  
Mean Aortic Pressure

The effect of altering hemodynamic parameters and blood milieu on myocardial oxygen extraction (O2E) was observed in an improved preparation of the anesthetized, open-chested dog. O2E remains at or near its high level for at least 40 min despite shifts in pH and cardiac input and sustained aortic compression. Aortic compression at constant cardiac input is associated with a moderate O2E decrease. Alternate aortic compression and release accompanied by induced shifts in pH and pCO2 caused an earlier and accelerated O2E decline. Coronary flow (CF) ordinarily is at a minimum for a given cardiac effort and rises when O2E declines. The O2E fall and CF increase are considered evidence of loss of coronary vascular tone. Despite shifts between CF and O2E, myocardial O2 consumption (O2C) remains closely associated with the cardiac effort index (mean aortic pressure x heart rate—HR·BP). Shifts in cardiac input, pH, and/or pCO2 have minimal effects on this O2C/HR·BP relationship. The significance of HR·BP as an energy utilization index is discussed.

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