Coronary vascular sympathetic beta-receptor innervation

1976 ◽  
Vol 230 (6) ◽  
pp. 1569-1576 ◽  
Author(s):  
FN Hamilton ◽  
EO Feigl
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Oxygen Tension ◽  
Coronary Sinus ◽  
Stellate Ganglion ◽  
Coronary Vessels ◽  
Coronary Perfusion ◽  
Receptor Blockade ◽  
Langendorff Preparation ◽  
Beta 2

Recent studies indicate that coronary vessels have alpha- and beta-2-adrenergic receptors and that the alpha receptors are functionally innervated. We studied whether the beta-2-vasodilator receptors are functionally innervated, using a dog in situ modified Langendorff preparation with constant coronary perfusion pressure. The beating, nonworking heart and systemic circulation were supported with a pump oxygenator. Stimulation of the left stellate ganglion increased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values. After beta-1-receptor blockade (practolol, 10 mg/kg), stellate stimulation decreased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values, revealing alpha-receptor vasoconstriction. After the addition of alpha-receptor blockade (Dibozane, 5 mg/kg), stellate stimulation increased coronary blood flow and coronary sinus oxygen tension a small amount from prestimulation values. Finally, after the addition of beta-2-receptor blockade (propranolol, 2 mg/kg), stellate stimulation increased flow and coronary sinus oxygen tension slightly from prestimulation control values. Direct intracoronary injections of isoproterenol, norepinephrine, and epinephrine gave results consistent with the presence of beta-1 myocardial receptors and alpha and beta-2 coronary receptors. We conclude that there is little functional innervation of coronary vascular beta-2 receptors. Intracoronary injections of isoproterenol and epinephrine activated beta-2-receptor coronary vasodilation after beta-1-receptor blockade, but norepinephrine did not.

Coronary blood flow changes following activation of adrenergic receptors in the conscious dog

1982 ◽  
Vol 243 (1) ◽  
pp. H13-H19 ◽  
Author(s):  
P. A. Gwirtz ◽  
H. L. Stone
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptors ◽  
Stellate Ganglion ◽  
Receptor Blockade ◽  
Circumflex Artery ◽  
Left Circumflex Artery ◽  
Left Stellate Ganglion ◽  
Before And After ◽  
Alpha Receptors ◽  
Beta 2

The role of coronary vascular adrenergic receptors in changing coronary flow was studied in dogs instrumented to measure left circumflex artery blood flow (CBF), mean coronary artery blood pressure (CBP), and heart rate (HR). Norepinephrine (NE), isoproterenol (IP), and phenylephrine (PH) were injected into the left circumflex artery before and after selective intracoronary alpha- and beta 1- or combined beta 1- and beta 2-receptor blockade. NE, IP, and PH did not alter CBP (112 +/- 6 mmHg). In addition, IP and PH did not affect HR (103 +/- 4 beats/min). NE increased HR to 150 +/- 6 beats/min, which was eliminated by blocking beta 1-receptors with atenolol and by removing the left stellate ganglion. IP increased CBF from 65 +/- 9 to 115 +/- 16 ml/min (mediated by both beta 1- and beta 2-receptors). PH caused an alpha-receptor-mediated coronary vasoconstriction (42 +/- 5 ml/min), which was potentiated by beta 1- and beta 2-receptor blockade. NE caused a biphasic flow response. CBF initially increased to 117 +/- 14 ml/min (mediated predominantly by beta 1-receptors) followed by a prolonged decrease to 54 +/- 7 ml/min (mediated by alpha-receptors). Removing the left stellate ganglion did not affect the CBF response to NE. These data indicate that PH directly stimulates coronary alpha-receptors and IP stimulates myocardial beta 1- and coronary beta 2-receptors. NE also stimulates myocardial cells causing a reflex that increases HR and indirectly increases CBF. The vasoconstriction to NE and PH was not evident after pentobarbital anesthesia, whereas the coronary vasodilation and increase in HR to NE was still present.

The coronary and luminal circulations of the myocardium of fishes

1991 ◽  
Vol 69 (7) ◽  
pp. 1993-2001 ◽  
Author(s):  
Peter S. Davie ◽  
Anthony P. Farrell
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Species Differences ◽  
Coronary Circulation ◽  
Venous Blood ◽  
Coronary Vessels ◽  
Coronary Perfusion ◽  
Environmental Hypoxia

There are two routes to supply oxygen to the myocardium of fishes, an oxygen-poor luminal supply and, in some fishes, an additional oxygen-rich coronary circulation. When present in teleost fishes, coronary vessels penetrate the myocardium to differing degrees. Elasmobranchs have coronary vessels throughout the myocardium. The different distributions of the coronary vessels reflect solutions to the problem of oxygen diffusion from the luminal blood to various parts of the heart, especially the outer layers of large ventricles. By examining cardiovascular data derived from in vivo experimental perturbations, such as exercise and environmental hypoxia, and from in vitro studies with perfused hearts, we discuss the extent to which luminal venous blood obviates the need for a coronary circulation and the extent to which the coronary circulation supplements the luminal oxygen supply. The oxygen content of the venous blood surpasses the maximal demand of the working heart and so the likely limitation of the luminal blood is the venous partial pressure of oxygen [Formula: see text] which in part determines the oxygen gradient to the mitochondria. The threshold venous [Formula: see text] is between 6 and 16 torr. Whether the coronary circulation is perfused in all species of fishes under resting conditions is not clear. Experimental data support the idea that there are species differences in the relative dependence on the coronary circulation. Coronary perfusion becomes relatively more important in situations where venous [Formula: see text] decreases and myocardial oxygen demand stays the same or increases, e.g., sustained aerobic exercise, environmental hypoxia, and the recovery period after exercise. Observations in vivo and in vitro support the idea that the pressure-generating potential of the heart, as opposed to the potential for flow output, is much more sensitive to changes in coronary blood flow. Coronary blood flow is more likely to be controlled through modulation of a large coronary vasodilatory reserve than through variations in perfusion pressure. Studies on coronary vasoactivity in fishes are limited; nonetheless, species differences are apparent.

Myocardial extraction of Rb86 in the rabbit

1959 ◽  
Vol 197 (6) ◽  
pp. 1175-1177 ◽  
Author(s):  
Robert E. Mack ◽  
David D. Nolting ◽  
Charles E. Hogancamp ◽  
Richard J. Bing
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Rabbit Heart ◽  
Myocardial Uptake ◽  
Langendorff Preparation ◽  
Average Value ◽  
Isolated Rabbit Heart

An investigation of the myocardial extraction of Rb86 was carried out using the Langendorff preparation in the isolated rabbit heart. Extraction was found to be related exponentially to both the rate of flow and the length of time of the flow. In the determination of coronary blood flow based upon the myocardial uptake of Rb86, an average value for myocardial extraction must be assumed in order to avoid coronary sinus catheterization. The data in these rabbit experiments suggest that when coronary blood flow is increased or decreased 50% the error which results from assuming a constant value for myocardial extraction is of the order of 20%.

Effects of Elevated Coronary Sinus Pressure on Coronary Blood Flow and Left Ventricular Function

Circulation ◽  
1995 ◽  
Vol 92 (9) ◽  
pp. 298-303 ◽  
Author(s):  
Takuya Miura ◽  
Takeshi Hiramatsu ◽  
Joseph M. Forbess ◽  
John E. Mayer
Keyword(s):  
Blood Flow ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Left Ventricular ◽  
Sinus Pressure

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.

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.

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.

Coronary hyperperfusion and myocardial metabolism in isolated and intact hearts

1987 ◽  
Vol 253 (5) ◽  
pp. H1271-H1278 ◽  
Author(s):  
W. P. Miller ◽  
N. Shimamoto ◽  
S. H. Nellis ◽  
A. J. Liedtke
Keyword(s):  
Blood Flow ◽  
Fatty Acid ◽  
Coronary Blood Flow ◽  
Myocardial Metabolism ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Rat Hearts ◽  
Heart Preparation ◽  
Significant Change ◽  
Lv Volume

We determined the independent influence of coronary hyperperfusion on myocardial metabolism in isolated and intact hearts. In an isovolumic blood-perfused rat heart preparation working against a left ventricular (LV) balloon, the effect of increasing coronary perfusion pressure from 100 to 150 mmHg was assessed. In three groups of rat hearts LV volume was fixed to obtain LV peak pressures of 42 +/- 3, 101 +/- 5, and 130 +/- 6 mmHg. With coronary hyperperfusion, LV pressure increased 27, 18, and 16%, LV maximum time derivative of pressure (dP/dt) increased 39, 20, and 22%, and myocardial O2 consumption (VO2) increased 16, 17, and 33%, respectively. In a fourth group, LV peak pressure was held constant at 92 +/- 4 mmHg during coronary hyperperfusion by decreasing LV volume. In this group, despite an increase in coronary blood flow of 48%, there was no significant difference in LV maximum dP/dt or myocardial VO2. Thus, in isolated rat hearts, coronary hyperperfusion was not an independent stimulus to myocardial VO2. To further test this, the effect of coronary hyperperfusion on myocardial metabolism was studied in an intact working swine heart preparation where the cardiac output was fixed with a right heart bypass circuit. Fatty acid oxidation in the left anterior descending bed was assessed by production of 14CO2 from [14C(U)]palmitate. A comparison of coronary perfusion 106 +/- 5 vs. 197 +/- 5 mmHg resulted in no significant change in global LV function, including LV internal diameter. Despite a 70% increase in coronary blood flow, there was no significant change in myocardial VO2 or fatty acid utilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Alpha 2-adrenoceptor stimulation can augment coronary vasodilation maximally induced by adenosine in dogs

1989 ◽  
Vol 257 (1) ◽  
pp. H132-H140 ◽  
Author(s):  
M. Hori ◽  
M. Kitakaze ◽  
J. Tamai ◽  
K. Iwakura ◽  
A. Kitabatake ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Small Dose ◽  
Reactive Hyperemia ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vasodilation ◽  
Beta Adrenoceptor ◽  
Adenosine Concentration ◽  
Hyperemic Flow

To determine whether alpha 2-adrenoceptor stimulation can augment adenosine-induced coronary vasodilation, 34 open-chest dogs were studied. When a small dose of clonidine (up to 0.24 micrograms.kg-1.min-1 ic) was administered under beta-adrenoceptor blockade, coronary blood flow [312 +/- 16 (SE) ml.100 g-1.min-1] maximally induced by intracoronary infusion of adenosine was further increased (P less than 0.05) by 66 +/- 16 ml.100 g-1.min-1, despite no significant changes in coronary perfusion pressure, myocardial oxygen consumption, and coronary venous adenosine concentration. However, when a larger dose of clonidine (0.36–0.60 micrograms.kg-1.min-1) was infused, adenosine-induced flow progressively decreased. This biphasic action of the alpha 2-adrenoceptor activity was also observed when the dose of norepinephrine was increased during alpha 1-adrenoceptor blockade with prazosin. Norepinephrine up to 0.24 micrograms.kg-1.min-1 (ic) further increased adenosine-induced coronary blood flow by 24 +/- 5% (P less than 0.001), whereas hyperemic flow was decreased by a larger dose of norepinephrine. In contrast to the alpha 2-adrenoceptor stimulation, the alpha 1-adrenoceptor stimulation (norepinephrine with yohimbine) progressively decreased coronary blood flow. Furthermore, with a small dose of clonidine, reactive hyperemic flow significantly increased compared with that without clonidine (303 +/- 13 vs. 355 +/- 13 ml.100 g-1.min-1, P less than 0.001), but a larger dose of clonidine adversely reduced reactive flow (254 +/- 18 ml.100 g-1.min-1, P less than 0.001). Adenosine release during reactive hyperemia with and without intracoronary infusions of clonidine were not altered significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Net Release

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

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