Canine coronary venous pressures: responses to positive inotropism and vasodilation

1983 ◽  
Vol 61 (3) ◽  
pp. 213-221 ◽  
Author(s):  
G. A. Klassen ◽  
J. A. Armour
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Systolic Pressure ◽  
Aortic Occlusion ◽  
Venous Tone ◽  
Coronary Veins ◽  
Artery Pressure ◽  
Intramyocardial Pressure ◽  
Positive Inotropism

The epicardial coronary venous pressure in 16 dogs was compared with coronary arterial pressure as well as aortic, intraventricular, and intramyocardial pressures. Partial aortic occlusion augmented intraventricular (IVP), intramyocardial (IMP), aortic (AP), and coronary arterial pressures. Peripheral coronary venous pressure was also elevated. Dobutamine significantly augmented IVP and IMP but not aortic or central coronary artery pressures; this agent significantly elevated coronary venous systolic pressure (28/8 to 84/12 mmHg) (1 mmHg = 133.322 Pa). Nitroglycerine decreased IVP, IMP, and AP significantly. Central coronary arterial pressure also fell significantly, but coronary venous pressures remained unchanged. In contrast dipyridamole resulted in no change in IVP, IMP, AP, or coronary arterial systolic pressures; however, the peripheral coronary venous systolic pressure became significantly elevated. Thus the two vasodilators, nitroglycerine and dipyridamole, had different effects upon coronary venous pressure. These data reinforce the recently expressed view that coronary veins behave in a complex fashion and further suggest that their pressures are dependent upon coronary artery pressure, intramyocardial pressure, and coronary venous tone.

Effect of hypoxia on pulmonary artery pressure of dogs

1964 ◽  
Vol 207 (6) ◽  
pp. 1314-1318 ◽  
Author(s):  
Benson R. Wilcox ◽  
W. Gerald Austen ◽  
Harvey W. Bender
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Systemic Hypoxia ◽  
Pump Output ◽  
Pulmonary Arterial

The mechanism by which the pulmonary artery pressure rises in response to hypoxia has never been clearly demonstrated. This problem was reinvestigated in experiments utilizing separate pulmonary and systemic perfusion systems. These vascular beds were perfused in such a fashion that a change in pulmonary artery pressure could only result from changes in vasomotor tone. Alveolar-pulmonary vein hypoxia was usually associated with a slight fall in pulmonary artery pressure. Systemic hypoxia resulted in elevation of pulmonary arterial pressure in 10 of the 12 animals tested with a constant-flow and constant-pulmonary venous pressure. In addition, all animals with systemic desaturation showed an increased venous return. When the "cardiac output" (pump output) was increased to match this return, the elevation in pulmonary artery pressure increased. It was concluded that the pulmonary arterial pressure elevation seen with hypoxia is the result of active pulmonary vasoconstriction coupled with an increased pulmonary blood flow.

Phasic characteristics of arterial inflow and venous outflow of right ventricular myocardium in dogs

1992 ◽  
Vol 262 (5) ◽  
pp. H1422-H1427 ◽  
Author(s):  
O. Hiramatsu ◽  
A. Kimura ◽  
T. Yada ◽  
T. Yamamoto ◽  
Y. Ogasawara ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Right Ventricular ◽  
Right Coronary Artery ◽  
Pulmonary Stenosis ◽  
Systolic Pressure ◽  
Laser Doppler Velocimeter ◽  
Venous Outflow ◽  
Coronary Veins ◽  
Arterial Inflow ◽  
The Right

To clarify the characteristics and causes of phasic blood flow in coronary circulation of the right ventricle we measured blood velocities in peripheral portions of the right coronary artery and vein in dogs under three conditions: control, transient pulmonary stenosis, and isoproterenol administration. An optical fiber sensor of a laser Doppler velocimeter was fixed onto the vessels (150-500 microns OD) with cyanoacrylate. The phasic pattern of distal arterial velocity was compared with the proximal velocity in the right coronary artery measured with an ultrasound pulsed Doppler velocimeter. Systolic-to-total velocity area ratio in the small epicardial artery [0.38 +/- 0.03 (SE)] was found to be smaller than in the large epicardial artery (0.51 +/- 0.02, P less than 0.01), indicating a capacitive filling of the epicardial artery during systole. The velocity waveform in small right coronary veins was predominantly systolic; i.e., it increased with a rise of right ventricular pressure and decreased with right ventricular relaxation. Comparison of the waveforms during isoproterenol infusion and pulmonary stenosis indicates that contraction of the ventricle is more important than right ventricular systolic pressure in retarding arterial inflow and accelerating venous outflow.

Epicardial coronary venous pressures: autonomic responses

1982 ◽  
Vol 60 (5) ◽  
pp. 698-706 ◽  
Author(s):  
G. A. Klassen ◽  
J. A. Armour
Keyword(s):  
Coronary Artery ◽  
Vagal Stimulation ◽  
Venous Pressure ◽  
Outflow Tract ◽  
The Other ◽  
Sympathetic Stimulation ◽  
Pressure Regulation ◽  
Autonomic Responses ◽  
Intramyocardial Pressure

Intramyocardial, ventricular, aortic, and central and peripheral coronary artery as well as peripheral and central coronary venous pressures were measured simultaneously in dog hearts. A gradient of coronary vascular pressures was detected and quantitated. Stellate stimulation increased all pressures. Isoproterenol induced outflow tract obstructions so that aortic and central coronary artery pressures were unchanged while the other pressures increased. Vagal stimulation dissociated the intramyocardial venous pressure relationship in as much as arterial pressures decreased while epicardial coronary venous pressure was increased. These data suggest that coronary venous pressure in response to sympathetic stimulation increases as intramyocardial pressure increases. However, vagal stimulation permits a dissociation of these effects suggesting that coronary venous pressure regulation is complex.

Cessation of arterial and venous flow at a finite driving pressure in porcine coronary circulation

1984 ◽  
Vol 246 (4) ◽  
pp. H525-H531 ◽  
Author(s):  
R. F. Bellamy ◽  
J. D. O'Benar
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Coronary Sinus ◽  
Time Course ◽  
Coronary Circulation ◽  
Venous Pressure ◽  
Pressure Change ◽  
Arterial Flow ◽  
Venous Flow ◽  
Artery Flow

We investigated the hypothesis that coronary capacitance is responsible for epicardial coronary artery flow stopping at arterial pressures greater than the coronary venous pressure. Using an in situ blood-perfused swine heart preparation, we compared the arterial pressures at which coronary artery inflow and coronary sinus outflow ceased. A pressure change was used that had the time course of aortic pressure during diastole. Data were obtained in hypocalcemic-arrested, adenosine-vasodilated preparations before and after pharmacologic interventions simulating the coronary circulation of the intact beating heart. The effect of extravascular compression was studied with barium contracture, while acetylcholine was infused to increase coronary vasomotor tone. The arterial pressure when arterial flow ceased was 13 +/- 5 mmHg in the arrested-vasodilated preparations, 37 +/- 10 mmHg after acetylcholine, and from 18 to 150 mmHg during barium contracture. Coronary sinus outflow ceased when arterial pressure was slightly less than the arterial pressure at which arterial flow had stopped. The differences between the arterial and venous zero flow arterial pressures were as follows: arrested-vasodilated 4 +/- 3 mmHg, acetylcholine 9 +/- 4, and barium contracture 0 +/- 3. The arteriovenous pressure gradients across the coronary bed at the instant venous flow ceased were as follows: arrested-vasodilated 5 +/- 6 mmHg, acetylcholine 23 +/- 6, and from 12 to 128 during barium contracture. These data do not support the suggestion that cessation of epicardial artery flow is solely a capacitance phenomenon.

scholarly journals Coronary venous retroperfusion: an old concept, a new approach

2008 ◽  
Vol 104 (5) ◽  
pp. 1266-1272 ◽  
Author(s):  
Ghassan S. Kassab ◽  
Jose A. Navia ◽  
Keith March ◽  
Jenny Susana Choy
Keyword(s):  
Myocardial Ischemia ◽  
Arterial Pressure ◽  
Clinical Utility ◽  
Myocardial Infarct ◽  
Venous Pressure ◽  
Coronary Veins ◽  
New Approach ◽  
Catheterization Laboratory ◽  
St Elevation ◽  
New Perspective

The potential of the coronary veins for revascularization has been evaluated by many investigators for more than a century. The major hurdle has been the damage of veins during sudden exposure to arterial pressure. The solution to this problem has typically involved the use of intricate and complicated apparatus and devices, which has prevented routine clinical utility in the catheterization laboratory. This review examines this old concept from a new perspective and proposes a novel hypothesis to address previous shortcomings. We speculate on an approach that may serve to eliminate the edema and hemorrhage that result during venous retroperfusion as the pressure is suddenly increased to arterial values. We propose the rationale to increase the venous pressure to arterial values more gradually to allow prearterializations of the veins before full exposure of arterial pressure. Finally, we discuss various possible indications for this selective autoretroperfusion strategy to combat myocardial ischemia in cardiogenic shock patients, ST-elevation myocardial infarct patients, no-option patients, and beyond.

Pressure and flow in epicardial coronary veins of the dog heart: responses to positive inotropism

1984 ◽  
Vol 62 (1) ◽  
pp. 38-48 ◽  
Author(s):  
J. A. Armour ◽  
G. A. Klassen
Keyword(s):  
Coronary Artery ◽  
Coronary Sinus ◽  
Venous Pressure ◽  
Stellate Ganglion ◽  
Canine Heart ◽  
Coronary Vein ◽  
Venous Flow ◽  
Coronary Veins ◽  
Coronary Sinus Flow ◽  
The Right

Peripheral coronary venous pressures and coronary sinus venous flow were measured in the canine heart as well as intramyocardial, intraventricular, aortic, and coronary artery pressures. Maximum coronary venous flow occurred after maximum intramyocardial and peripheral coronary artery pressures had been reached. Maximum venous flow occurred at or following the maximum peripheral coronary vein pressure. Positive inotropic changes induced by stimulation of the right or left stellate ganglia or infusing isoproterenol, norepinephrine, or dobutamine significantly increased intramyocardial pressure, systolic epicardial coronary venous pressure, and systolic coronary venous flow. Mean coronary sinus flow was augmented by all interventions except isoproterenol. The estimated systolic vein resistance was slightly increased following right stellate ganglion stimulation, but not following left stellate ganglion stimulation, isoproterenol, or dobutamine. Norepinephrine reduced this parameter minimally. These data indicate that coronary veins respond differently to a variety of different positive inotropic interventions.

Epicardial coronary venous pressure

1981 ◽  
Vol 59 (12) ◽  
pp. 1250-1259 ◽  
Author(s):  
J. A. Armour ◽  
G. A. Klassen
Keyword(s):  
Coronary Artery ◽  
Coronary Sinus ◽  
Pressure Wave ◽  
Venous Pressure ◽  
Side Branch ◽  
Canine Heart ◽  
Coronary Vein ◽  
Intramyocardial Pressure ◽  
Wave Forms ◽  
Peak Pressures

Coronary venous pressure was measured in two sites in the canine heart. Central coronary venous pressure was that pressure recorded by a catheter in an epicardial coronary vein directed antegrade towards the coronary sinus. This pressure was 6 ± 1/0.2 ± 0.6 mmHg (1 mmHg = 133.322 Pa). Peripheral coronary venous pressure was recorded by a catheter in an epicardial vein which was directed towards the apex. It was 27 ± 5/8 ± 2 mmHg. Simultaneous measurement of peripheral coronary artery and vein pressures demonstrated similar pressure wave forms with peak pressures during systole. Peripheral coronary venous pressure was similar if measured from a side branch leading to the major epicardial veins or via a catheter placed retrograde in a major epicardial vein. Thus artifact of measurement caused by antegrade catheter placement was negligible. During norepinephrine administration, venous pressures were significantly increased. These data suggest that coronary venous pressures are higher than is generally assumed and that intramyocardial pressure has an important effect upon coronary venous pressure.

Physiological Factors Influencing Pulmonary Artery Pressure During Separate Perfusion of the Systemic and Pulmonary Circulations in the Dog

1957 ◽  
Vol 191 (3) ◽  
pp. 453-460 ◽  
Author(s):  
Peter Weil ◽  
Peter F. Salisbury ◽  
David State
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Ventilation ◽  
Venous Pressure ◽  
Air Embolism ◽  
Systemic Circulation ◽  
Systemic Arterial Pressure ◽  
Artery Pressure ◽  
Physiological Variables

An open-chest dog preparation is described in which the systemic circulation is perfused by a heart-lung machine and the lesser circulation is perfused by a pump-reservoir circuit. In this preparation there is no connection between the two circulations other than the bronchial flow; the flow in the pulmonary vessels is known and controlled at all times. The influence of physiological variables on pulmonary artery pressure was investigated and the results of earlier investigations were confirmed with reference to pressure-flow relationships, the effect of changes in pulmonary ventilation (in part), the inhalation of CO2, pulmonary air embolism, the lack of effect of changes of systemic arterial pressure. Increases of systemic venous pressure caused simultaneous increases of pulmonary arterial pressure.

Coronary venous pressure and flow: effects of vagal stimulation, aortic occlusion, and vasodilators

1984 ◽  
Vol 62 (5) ◽  
pp. 531-538 ◽  
Author(s):  
G. A. Klassen ◽  
J. A. Armour
Keyword(s):  
Coronary Artery ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Canine Heart ◽  
Mean Flow ◽  
Venous Flow ◽  
Intramyocardial Pressure ◽  
Coronary Sinus Flow ◽  
Venous Resistance ◽  
Flow Effects

Coronary venous pressure and coronary sinus flow in the canine heart were compared with intramyocardial, intraventricular, aortic, and coronary artery pressures. Stimulation of the thoracic vagus augmented coronary venous pressure, mean venous flow per systole, and coronary venous systolic resistance, but decreased the mean venous flow. Partial occlusion of the aorta augmented coronary venous pressure and coronary venous flow, while systolic coronary venous resistance remained unchanged. Adenosine increased peripheral and central coronary venous pressure and venous flow; it reduced peripheral coronary artery presure. Adenosine augmented flow per systole and reduced venous resistance more than the other interventions. Dipyridamole decreased left ventricular, aortic, and central coronary artery systolic pressures and systolic venous resistance. It increased the venous flow, mean flow per systole, and coronary venous pressure, even though intramyocardial pressure remained unchanged. Nitroglycerine elevated coronary venous pressure and flow, as well as venous flow per systole, even though it decreased left ventricular, aortic, and central coronary artery pressures. Nitroglycerine significantly decreased coronary venous resistance. It is concluded that coronary venous resistance may be an important resistive component to consider when the total coronary circulation is studied.

Coronary artery compliance in the dog

1982 ◽  
Vol 60 (7) ◽  
pp. 942-951 ◽  
Author(s):  
G. A. Klassen ◽  
A. Y. K. Wong
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Coronary Flow ◽  
Arterial Wall ◽  
Coronary Circulation ◽  
Stellate Ganglion ◽  
Sympathetic Stimulation ◽  
Intramyocardial Pressure ◽  
Left Stellate Ganglion

Measurement of left anterior descending coronary arterial pressure, phasic coronary flow, and intramyocardial pressure in an open-chest dog provided data, which when entered into the computer model of the coronary circulation, permitted calculation of coronary artery compliance and resistance during systole and diastole. Resting in vivo compliance averaged 0.21 × 10−3 mL/mmHg (1 mmHg = 133.322 Pa) while systolic resistance averaged 4.05 mmHg∙min−1∙mL−1 and during diastole 2.06 mmHg∙min−1∙mL−1. Left stellate ganglion stimulation or vasodilation caused minimal changes in compliance but glutaraldehyde applied to arterial wall caused a decrease in compliance. Sympathetic stimulation and vasodilation decreased both diastolic and systolic resistance. Transmural distribution of coronary flow was not significantly altered by the experimental changes in compliance and resistance.

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