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.

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.

Pattern of blood flow in the pulmonary veins of the dog

1965 ◽  
Vol 20 (6) ◽  
pp. 1118-1128 ◽  
Author(s):  
Eugene Morkin ◽  
John A. Collins ◽  
Harold S. Goldman ◽  
Alfred P. Fishman
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Pulmonary Veins ◽  
Electromagnetic Flowmeter ◽  
Sine Wave ◽  
Left Ventricular ◽  
Mean Flow ◽  
Venous Flow ◽  
Pulmonary Venous Flow ◽  
Atrial Contraction

The pattern of blood flow in the large pulmonary veins was studied in dogs by chronic implantation of sine-wave electromagnetic flowmeters and cineangiographic observations. These revealed that: 1) pulmonary venous flow is continuous and pulsatile with peak rate of flow of approximately twice the mean flow; 2) the initial rapid increase in venous flow occurs 0.10 sec after the onset of ventricular systole, reaching a peak at the time of closure of the A-V valves; 3) left atrial contraction produces a fleeting slowing or reversal of flow; and 4) respiratory variations in pulmonary venous flow follow those in pulmonary arterial flow, beat by beat. The genesis of phasic pulmonary venous flow was investigated by analysis of pressure and flow curves from the two sides of the heart, by consideration of the energy required for left ventricular filling, and by reconstruction of the pulmonary venous flow pulse using a mathematical model of the pulmonary circulation. These three lines of evidence are consistent in indicating that the transmitted right ventricular pressure is the major determinant of the pulmonary venous flow pattern in the dog. pulsatile pulmonary venous flow; pulmonary venous flow; pulmonary circulation; ventricular suction; respiration on pulmonary circulation; pulmonary venous angiography; pulmonary veno-atrial junctions; electromagnetic flowmeter; cineangiography Submitted on November 16, 1964

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 histamine on coronary microvascular permeability

1984 ◽  
Vol 247 (1) ◽  
pp. H1-H7 ◽  
Author(s):  
C. F. Pilati ◽  
M. B. Maron
Keyword(s):  
Heart Rate ◽  
Vascular Permeability ◽  
Autologous Blood ◽  
Venous Pressure ◽  
Apparent Volume ◽  
Left Ventricular ◽  
Canine Heart ◽  
Blood Proteins ◽  
Plasma Protein Concentration ◽  
Ventricular Performance

The effect of histamine on coronary vascular permeability was assessed under conditions of elevated venous pressure in the spontaneously beating, isolated canine heart perfused with autologous blood. The apparent volume of fluid filtered from the vasculature to the interstitium (VF) was calculated from the increase in plasma protein concentration and also from the increase in hematocrit. The ratio of the protein-filtered volume to the hematocrit-filtered volume (VF,Pr/VF,Hct) was used to evaluate changes in permeability. In the absence of histamine, the VF,Pr/VF,Hct was near unity (1.05 +/- 0.11), which indicated that the blood proteins and the red blood cells had concentrated equally. Thus the transudate was essentially protein free. On exposure to histamine (3.8 +/- 0.3 microgram base/ml blood), VF,Pr/VF,Hct decreased to 0.37 +/- 0.06 (P less than 0.001), which indicated that coronary vascular permeability had increased. This value remained constant throughout the 60 min of histamine exposure. Aortic perfusion pressure decreased significantly (P less than 0.05) from 111 +/- 11 to 84 +/- 5 mmHg during the 1st min of histamine exposure and rose slowly thereafter. In four of the seven hearts, concomitant increases in left ventricular isovolumic pressure development (13-31 mmHg) and heart rate (4-29 beats/min) were observed. In the remaining hearts, neither variable was affected by histamine. We conclude that histamine causes an increase in the permeability of the canine coronary microvasculature but fails to increase heart rate or left ventricular performance consistently.

Image-Based Modeling of Blood Flow in Human Coronary Arteries With and Without Bypass Grafts During Rest and Simulated Exercise

2008 ◽  
Author(s):  
Jessica Shih ◽  
Hyun Jin Kim ◽  
Charles A. Taylor
Keyword(s):  
Coronary Artery ◽  
Coronary Bypass ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Bypass Grafts ◽  
Heart Model ◽  
Intramyocardial Pressure ◽  
Image Based Modeling ◽  
Lumped Parameter

The number of patients with coronary artery disease continues to rise, with approximately 469,000 coronary bypass procedures in 2005 alone [1]. A priori knowledge of the flow features within the coronary vascular system could prove useful in predicting flow changes due to coronary bypass surgery. Image-based modeling and 3-D computational simulations could be used to compute flow and pressure in a patient-specific manner. However, modeling coronary flow requires knowledge of the intramyocardial pressure that compresses coronary vessels, resulting in decreased flow in systole and increased flow in diastole. Left ventricular pressure can provide an estimate to intramyocardial pressure, but the aortic pressure and left ventricular pressure must be coupled in systole when the aortic valve is open. Previously, we have developed a method to couple a lumped-parameter heart model to the inlet of a 3-D model to compute aortic and ventricular pressure [2]. In this study, we use the lumped-parameter heart model and computational fluid dynamics to calculate flow dynamics in a patient model with coronary artery bypass grafts.

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.

Hepatic venular pressures of rats, dogs, and rabbits

1991 ◽  
Vol 261 (3) ◽  
pp. G539-G547 ◽  
Author(s):  
H. G. Bohlen ◽  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Inferior Vena Cava ◽  
Portal Vein ◽  
Inferior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Norepinephrine Infusion ◽  
Venous Resistance ◽  
Venous Vasculature

We tested the hypotheses that the hepatic venule pressures (Phv), just downstream from the hepatic sinusoids, are closely similar (less than 2 mmHg) either to the portal venous pressure (Ppv), indicating a high hepatic venous resistance, or to the inferior vena cava (Pivc) pressure, indicating a high portal-sinusoidal venous resistance, as reported by previous investigators. A micropipette servo-null pressure measurement technique was used with rats, dogs, and rabbits. Phv, referred to the anatomic level of the vena cava, averaged 5.1 +/- 1.0, 6.4 +/- 1.1, and 5.4 +/- 1.0 (SD) mmHg in the rats, puppies, and rabbits, respectively. Ppv averaged 8.0 +/- 1.4, 10.8 +/- 2.2, and 7.4 +/- 1.5 mmHg, respectively. Norepinephrine infusion into the portal vein (1-5 micrograms.min-1.kg-1) caused Ppv to increase and the portal venous flow to decrease but did not significantly affect Phv. The hepatic venous circuit contributed 44 +/- 17% (rats) and 31 +/- 26% (dogs) of the total liver venous vascular resistance under control conditions. We conclude that the portal and sinusoidal vasculatures are the dominant, but not exclusive, resistance sites of the liver venous vasculature both at rest and during norepinephrine-induced vasoconstriction.

Hemodynamic and Energetic Assessment of Calves Implanted with a Left Ventricular Assist Device (LVAD)

1988 ◽  
Vol 11 (2) ◽  
pp. 119-126 ◽  
Author(s):  
G.M. Pantalos ◽  
J.D. Marks ◽  
J.B. Riebman ◽  
N.A. Burton ◽  
R. Depaulis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Left Ventricular ◽  
Control Mode ◽  
Mean Flow ◽  
Assist Device ◽  
Ventricular Assist ◽  
Intramyocardial Pressure ◽  
Ventricular Assistance ◽  
Left Ventricular Assistance

Hemodynamic and ventricular energetic parameters were measured in calves implanted with the air driven Utah Ventricular Assist Device (UVAD). Uptake site was varied to determine the effect of control mode and vacuum augmentation of filling. Uptake was drawn solely from the left atrium or combined with a left ventricular apical vent. LVAD outflow returned to the descending, thoracic aorta. Control modes examined included asynchronous pumping as well as 1:1 and 1:2 synchronous diastolic counterpulsation. The 85cc LVAD, vacuum formed from PELLETHANE®, was implanted acutely in four animals and chronically in six (7, 49 and 116 days paracorporeally, 1, 28 and 32 days intrathoracically). Instantaneous blood pressures, intramyocardial pressure, aortic outflow, oxygen consumption, LVAD output and drive parameters were recorded. LVAD output was independent of control mode when the natural heart rate was ≥ 80 beats per minute. Intrathoracically positioned LVADs pumped a mean flow of ≈5 liters/min without vacuum augmentation of filling. Paracorporeally positioned LVADs pumped ≈3 liters/min mean flow without vacuum augmentation and up to ≈6 liters/min with 38 mm Hg of vacuum augmentation of filling. Instantaneous ascending aortic pressure and flow showed distinct beat-to-beat variation depending on LVAD control mode. Lower average ventricular afterload was observed when pumping the LVAD asynchronously or 1:2 synchronously. In one acute preparation, left ventricular myocardial oxygen consumption was reduced from the unassisted average control level by 37% for the asynchronous and 1:1 synchronous control modes with left atrial uptake. With combined uptake, oxygen consumption was reduced an additional 30% during asynchronous control or 11% during 1:1 synchronous control without any change in LVAD output. Endocardial/epicardial blood flow ratio was similar and ≥1.12 for all test conditions. Renal and brain blood flow was maintained, or slightly elevated during ventricular assistance. Intramyocardial pressures were monitored using Millar catheter tip transducers. In an acute preparation, left ventricular assistance reduced peak intramyocardial pressure. Changing from atrial to combined uptake cannulation further reduced peak intramyocardial pressure for asynchronous and 1:1 synchronous LVAD control. Reduced end-diastolic intramyocardial pressures were seen with all modes of LVAD control. These data demonstrate excellent UVAD pumping function and suggest that left ventricular assistance does not compromise endocardial blood flow while sustaining blood flow to other major organs. Regardless of the uptake site, asynchronous or 1:2 synchronous LVAD control may be clinically preferable for effective reduction of left ventricular myocardial oxygen consumption.

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