Neuropeptide Y and coronary vasoconstriction: role of thromboxane A2

1992 ◽  
Vol 263 (4) ◽  
pp. H1045-H1053
Author(s):  
S. E. Martin ◽  
J. T. Kuvin ◽  
S. Offenbacher ◽  
B. M. Odle ◽  
R. E. Patterson
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Neuropeptide Y ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Thromboxane A2 ◽  
Coronary Resistance ◽  
Txa2 Receptor

We previously reported that coronary constriction following neuropeptide Y (NPY) was alleviated by cyclooxygenase blockade. To determine the role of thromboxane A2 (TxA2), anesthetized dogs received two paired doses of NPY given 2 h apart. Nine control dogs received NPY alone. Nine test dogs received one of three TxA2 receptor antagonists given between the doses of NPY. Also, five dogs received NPY during which prostaglandins were measured. In controls, NPY decreased coronary blood flow and increased aortic pressure; coronary resistance was increased significantly. Heart rate fell, and myocardial oxygen consumption was unchanged. Thromboxane receptor blockers significantly relieved the coronary constrictor effect of NPY. The reduction in coronary blood flow was blunted, while heart rate, first derivative of left ventricular pressure, and myocardial oxygen consumption were unchanged. Alleviation by TxA2 receptor blockade paralleled that reported for cyclooxygenase inhibitors. Also, significant increases in coronary venous TxA2 were seen at the time of maximal increases in coronary resistance, while prostacyclin was unchanged. In summary, TxA2 appears to mediate part of the coronary constrictor effect of NPY.

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.

Role of adenosine in norepinephrine-induced coronary vasodilation

1997 ◽  
Vol 273 (2) ◽  
pp. H557-H565 ◽  
Author(s):  
R. Van Bibber ◽  
D. W. Stepp ◽  
K. Kroll ◽  
E. O. Feigl
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Adenosine Receptor ◽  
Myocardial Oxygen Consumption ◽  
Temporal Correlation ◽  
Distributed Model ◽  
Receptor Blockade ◽  
Adenosine Concentration

Adenosine has been postulated to be the physiological transmitter coupling increases in coronary blood flow to increases in myocardial metabolism. The purpose of this experiment was to evaluate the role of adenosine in the coronary hyperemia due to norepinephrine. In 11 anesthetized, closed-chest canine preparations, the left main coronary artery was cannulated and perfused with blood at 100 mmHg. Coronary blood flow and myocardial oxygen consumption were measured, and interstitial adenosine concentration was estimated from arterial and coronary venous measurements using a distributed model. Adenosine receptor blockade with 8-phenyltheophylline (8-PT) was used to shift the adenosine dose-response curve 12-fold. During intracoronary norepinephrine infusion, coronary blood flow and myocardial oxygen consumption increased similarly before and after 8-PT, demonstrating a lack of an effect from the adenosine receptor blockade. Before 8-PT, estimated interstitial adenosine increased to a vasoactive concentration (220 nM); however, the temporal correlation with coronary blood flow was poor. After 8-PT, a similar increase in estimated interstitial adenosine was found, demonstrating that there was no augmentation in adenosine concentration to overcome the adenosine receptor blockade. Thus adenosine could not be responsible for the increase in coronary blood flow after adenosine receptor blockade and therefore is not required for norepinephrine-induced hyperemia.

Role of adenosine in local metabolic coronary vasodilation

1999 ◽  
Vol 276 (5) ◽  
pp. H1425-H1433 ◽  
Author(s):  
Toyotaka Yada ◽  
Keith Neu Richmond ◽  
Richard van Bibber ◽  
Keith Kroll ◽  
Eric O. Feigl
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Adenosine Receptor ◽  
Myocardial Oxygen Consumption ◽  
Receptor Blockade ◽  
Coronary Vasodilation ◽  
Paired Pulse ◽  
Adenosine Concentration

Adenosine has been postulated to mediate the increase in coronary blood flow when myocardial oxygen consumption is increased. The aim of this study was to evaluate the role of adenosine when myocardial oxygen consumption was augmented by cardiac paired-pulse stimulation without the use of catecholamines. In 10 anesthetized closed-chest dogs, coronary blood flow was measured in the left circumflex coronary artery, and myocardial oxygen consumption was calculated using the arteriovenous oxygen difference. Cardiac interstitial adenosine concentration was estimated from coronary venous and arterial plasma adenosine measurements using a previously described multicompartmental, axially distributed mathematical model. Paired stimulation increased heart rate from 55 to 120 beats/min, increased myocardial oxygen consumption 104%, and increased coronary blood flow 92%, but the estimated interstitial adenosine concentration remained below the threshold for coronary vasodilation. After adenosine-receptor blockade with 8-phenyltheophylline (8-PT), coronary blood flow and myocardial oxygen consumption were not significantly different from control values. Paired-pulse pacing during adenosine-receptor blockade resulted in increases in myocardial oxygen consumption and coronary blood flow similar to the response before 8-PT. Coronary venous and estimated interstitial adenosine concentration did not increase to overcome the adenosine blockade by 8-PT. These results demonstrate that adenosine is not required for the local metabolic control of coronary blood flow during pacing-induced increases in myocardial oxygen consumption.

Adenosine and coronary blood flow in conscious dogs during normal physiological stimuli

1982 ◽  
Vol 243 (4) ◽  
pp. H628-H633 ◽  
Author(s):  
A. N. Bacchus ◽  
S. W. Ely ◽  
R. M. Knabb ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Oxygen Supply ◽  
Physiological Mechanism ◽  
Oxygen Demand ◽  
The Relationship ◽  
Chronically Instrumented Dogs

The role of adenosine in matching myocardial oxygen supply to demand by regulating coronary blood flow has been the subject of intensive study. The present experiments were designed to determine the relationship among myocardial oxygen consumption, coronary blood flow, and adenosine production as estimated by pericardial adenosine accumulation under several physiological conditions in the same animal. Conscious chronically instrumented dogs were used to measure changes in coronary blood flow, myocardial oxygen consumption, and pericardial adenosine accumulation during two levels of treadmill exercise, excitement caused by loud noises, and feeding (the presentation and consumption of a meal). The results show significant increases in the adenosine production with all experimental procedures and significant linear correlations between myocardial oxygen consumption and coronary blood flow (r = 0.78), myocardial oxygen consumption and adenosine production (r = 0.73), and adenosine production and coronary blood flow (r = 0.88). These data show that increases in adenosine production by the normally oxygenated myocardium can be the physiological mechanism for matching oxygen supply to increased oxygen demand in the conscious dog.

Left ventricular heat production during induced tachycardia in the intact dog

1965 ◽  
Vol 209 (1) ◽  
pp. 33-36 ◽  
Author(s):  
Skoda Afonso ◽  
David H. McKenna ◽  
George S. O'Brien ◽  
George G. Rowe ◽  
Charles W. Crumpton
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Metabolic Rate ◽  
Coronary Blood Flow ◽  
Heat Production ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Metabolic Parameters ◽  
Heat Control

It is well established that heart rate is a determinant of myocardial oxygen consumption. However, it has not been demonstrated that the increase of oxygen consumption at faster rates actually represents loss of energy, degraded as heat. Control measurements of systemic and coronary hemodynamic and metabolic parameters and left ventricular heat production (measured by a recently reported method) were obtained in 10 dogs. Tachycardia was then induced electrically and the same parameters redetermined. Significant increases occurred in coronary blood flow, cardiac metabolic rate of oxygen, and left ventricular heat production. The elevated myocardial oxygen consumption at higher rates is associated with increased heat production.

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.

Effect of aminophylline on coronary functional hyperemia and myocardial adenosine

1982 ◽  
Vol 243 (3) ◽  
pp. H480-H487 ◽  
Author(s):  
C. E. Jones ◽  
T. W. Hurst ◽  
J. R. Randall
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Functional Hyperemia ◽  
Intracoronary Infusion ◽  
Norepinephrine Infusion ◽  
Adenosine Antagonist

The role of adenosine in coronary functional hyperemia was tested using the adenosine antagonist aminophylline. In 11 dogs left coronary blood flow (LCBF) and left ventricular oxygen extraction [(a-v)O2] were monitored. Myocardial oxygen consumption (MVO2) was calculated. Before aminophylline was administered, intracoronary infusion of 6.8 micrograms/min norepinephrine increased LCBF and MVO2 by 40-80%. Simultaneous infusion of adenosine further increased LCBF. Fifteen minutes after injection of 100 mg aminophylline, norepinephrine still increased LCBF, and the ratio delta LCBF/delta MVO2 was unchanged (P greater than 0.05). Although the functional hyperemia was not blunted, the response to infused adenosine was abolished by aminophylline. In 20 additional dogs myocardial adenosine was determined. Before norepinephrine infusion myocardial adenosine with and without aminophylline was 12.7 and 14.3 nmol/g dry wt, respectively (P greater than 0.05). During norepinephrine infusion an increase in adenosine correlated well with increases in MVO2 and LCBF, but the increase in adenosine was not greater after aminophylline. Thus the failure of aminophylline to blunt functional hyperemia was not due to a higher adenosine level after aminophylline. These results do not support a role for adenosine in functional hyperemia elicited by norepinephrine.

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.

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