Effects of hydrodynamic forces on coronary production of prostacyclin and purines

1989 ◽  
Vol 256 (6) ◽  
pp. H1532-H1538 ◽  
Author(s):  
E. Karwatowska-Prokopczuk ◽  
G. Ciabattoni ◽  
A. Wennmalm
Keyword(s):  
Steady Flow ◽  
Flow Rate ◽  
Pulsatile Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Rabbit Heart ◽  
Phospholipase Activity ◽  
Specific Mechanism ◽  
Coronary Pressure ◽  
Prostacyclin Production

Prostacyclin and purine efflux rates from the isolated rabbit heart in response to variations of flow rate or perfusion pressure were investigated. Increases in coronary flow by 25, 50, and 100% augmented the effluxes of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and purines equally, by up to four times. Increases in coronary pressure by 25, 50, and 100% augmented the outflow of 6-keto-PGF1 alpha by up to 20 times, whereas the outflow of purines increased no more than 6.5 times. Neither reduction of perfusate Ca2+ by 50% nor administration of quinacrine (1 microM) affected the basal efflux of 6-keto-PGF1 alpha or its response to an increase in coronary pressure. Both interventions did, however, reduce the pressure-induced purine efflux by approximately 50%. Pulsatile flow did not affect either the outflow of 6-keto-PGF1 alpha or that of purines, in comparison to steady flow at the same rate. The data demonstrate that an increase in coronary pressure activates a specific mechanism for prostacyclin production that appears independent of extracellular Ca2+ and of phospholipase activity.

Coronary sinus pressure has a direct effect on gradient for coronary perfusion

1990 ◽  
Vol 258 (6) ◽  
pp. H1739-H1744 ◽  
Author(s):  
K. W. Scheel ◽  
S. E. Williams ◽  
J. B. Parker
Keyword(s):  
Coronary Sinus ◽  
Coronary Flow ◽  
Collateral Circulation ◽  
Perfusion Pressure ◽  
Coronary Vessels ◽  
Coronary Perfusion ◽  
Direct Influence ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Sinus Pressure

In previous work from this laboratory we demonstrated that the coronary pressure-flow relationship exhibits a zero pressure intercept in the absence of the influence of the collateral circulation. In the present study we determined the effect of varying coronary sinus pressures on coronary perfusion. Specifically, we investigated whether coronary flow would cease when the coronary inflow pressure equaled the coronary sinus pressure. The study was performed while inflow perfusion pressure to all coronary vessels was changed simultaneously in order to reduce the influence of the collateral circulation while coronary sinus outflow was measured. Coronary pressure-flow relationships were obtained for coronary sinus pressures of 0, 10, and 20 mmHg. The results demonstrate a strong correlation between perfusion pressure and coronary sinus pressure (r2 = 0.994 +/- 0.001), which passed through the origin. We conclude that coronary sinus pressures between 0 and 20 mmHg have a direct influence on coronary perfusion.

Hemodynamics of coronary artery stenosis

1984 ◽  
Vol 62 (1) ◽  
pp. 59-69 ◽  
Author(s):  
Alan Y. K. Wong ◽  
G. A. Klassen ◽  
David E. Johnstone
Keyword(s):  
Coronary Artery ◽  
Flow Rate ◽  
Pressure Loss ◽  
Coronary Flow ◽  
Cardiac Cycle ◽  
Low Flow ◽  
Published Data ◽  
Mean Flow ◽  
Additional Pressure ◽  
Coronary Pressure

A model is proposed to study the hemodynamics of various types of coronary stenosis. The model coronary artery is assumed to be an elastic tapered tube. A progressive degree of concentric and eccentric stenoses are studied. Measured pulsatile coronary pressure, flow, and intramyocardial pressure are used as input data to calculate the pressure and flow velocities at different locations of the artery. The simulation yields results that agree well with published data in dog experiments, and those from human stenotic coronary arteries. The present model shows that in a cardiac cycle, the overall hydraulic resistance owing to a specific stenosis tends to be flow independent at low flow rate but increases linearly with flow at higher coronary flow. This flow independent resistance increases with progressive stenosis. At low flow, the mean coronary flow in a cardiac cycle is relatively constant with stenoses up to 80%, but decreases dramatically with further increase in the degree of narrowing. At high resting flow rate, this mean flow is markedly reduced at much smaller degrees of constriction. The simulated pressure velocity relation of poststenotic dilatation indicates an additional pressure loss at the distal end of the stenosis, but the calculated resistance to flow is actually lessened. While stenosis length increases pressure loss and resistance to flow, its effect on mean flow appears disproportionally insignificant. Eccentric lesions appear to be more detrimental than concentric ones as they produce additional pressure loss and greater resistance across the coronary artery lesion.

PERFUSION PRESSURE IN RELATION TO THE PRODUCTION AND CESSATION OF EXPERIMENTAL CARDIAC ARRHYTHMIAS

1964 ◽  
Vol 42 (1) ◽  
pp. 21-24 ◽  
Author(s):  
J.-C. Panisset ◽  
R. Carle ◽  
A. Beaulnes
Keyword(s):  
Ventricular Fibrillation ◽  
Firing Rate ◽  
Cardiac Arrhythmias ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Rabbit Heart ◽  
Effect Of Pressure ◽  
Isolated Rabbit Heart ◽  
Myocardial Temperature ◽  
Low Pressures

The influence of perfusion pressure on ventricular fibrillation was studied in the isolated rabbit heart. Sudden drops in perfusion pressure inhibit ventricular fibrillation in a few minutes, whereas a slow decrease of the pressure does not stop the fibrillation, but nevertheless reduces the ventricular firing rate. High perfusion pressures facilitate the induction of fibrillation; low pressures delay the production of arrhythmias and shorten their duration. It is postulated that this effect of pressure is primarily mechanical and not strictly dependent upon changes in the coronary flow or in the myocardial temperature.

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.

A particle image velocimetry study on the pulsatile flow characteristics in straight tubes with an asymmetric bulge

2000 ◽  
Vol 214 (5) ◽  
pp. 655-671 ◽  
Author(s):  
S C M Yu ◽  
J B Zhao
Keyword(s):  
Particle Image Velocimetry ◽  
Steady Flow ◽  
Pulsatile Flow ◽  
Flow Condition ◽  
Particle Image ◽  
Flow Characteristics ◽  
Reynolds Numbers ◽  
Working Fluid ◽  
Flow Conditions ◽  
Image Velocimetry

Flow characteristics in straight tubes with an asymmetric bulge have been investigated using particle image velocimetry (PIV) over a range of Reynolds numbers from 600 to 1200 and at a Womersley number of 22. A mixture of glycerine and water (approximately 40:60 by volume) was used as the working fluid. The study was carried out because of their relevance in some aspects of physiological flows, such as arterial flow through a sidewall aneurysm. Results for both steady and pulsatile flow conditions were obtained. It was found that at a steady flow condition, a weak recirculating vortex formed inside the bulge. The recirculation became stronger at higher Reynolds numbers but weaker at larger bulge sizes. The centre of the vortex was located close to the distal neck. At pulsatile flow conditions, the vortex appeared and disappeared at different phases of the cycle, and the sequence was only punctuated by strong forward flow behaviour (near the peak flow condition). In particular, strong flow interactions between the parent tube and the bulge were observed during the deceleration phase. Stents and springs were used to dampen the flow movement inside the bulge. It was found that the recirculation vortex could be eliminated completely in steady flow conditions using both devices. However, under pulsatile flow conditions, flow velocities inside the bulge could not be suppressed completely by both devices, but could be reduced by more than 80 per cent.

Improvement in ischemic myocardial blood flow following a new calcium antagonist

1980 ◽  
Vol 239 (2) ◽  
pp. H163-H171 ◽  
Author(s):  
S. R. Jolly ◽  
G. J. Gross
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Aortic Pressure ◽  
Contractile Force ◽  
Tissue Blood Flow ◽  
Coronary Pressure ◽  
Ischemic Tissue ◽  
High Doses ◽  
Mean Aortic Pressure ◽  
Aortic Perfusion

The effect of FR 7534, a new dihydropyridine CA2+ antagonist, nitroglycerin, and dipyridamole have been compared on coronary collateral function in pentobarbital-anesthetized open-chest dogs following acute ligation of the left anterior descending coronary artery. Measurements of tissue blood flow using radioactive microspheres were made 60 min postligation after low and high doses of each drug and at the higher dose with methoxamine added to to return mean aortic pressure. FR 7534 treatment increased subepicardial, subendocardial, and transmural tissue flow by 100% in the central ischemic zone when perfusion pressure was controlled by methoxamine. Nitroglycerin also increased ischemic tissue flow, but to a lesser degree, 18% transmurally. Dipyridamole produced no significant change. Tissue flow in normal myocardium was similarly increased by FR 7534 and dipyridamole but slightly reduced by nitroglycerin. FR 7534 and nitroglycerin also increased retrograde coronary pressure when aortic presure was maintained constant. FR 7534, but not nitroglycerin, increased ischemic contractile force. In this model, FR 7534 may produce greater effects than nitroglycerin in increasing blood supply to ischemic myocardium delivered by endogenous collaterals especially when aortic perfusion pressure was controlled.

Factors regulating basal metabolism of the isolated perfused rabbit heart

1986 ◽  
Vol 250 (6) ◽  
pp. H998-H1007 ◽  
Author(s):  
C. L. Gibbs ◽  
G. Kotsanas
Keyword(s):  
Metabolic Rate ◽  
Coronary Flow ◽  
Constant Pressure ◽  
Rabbit Heart ◽  
Basal Metabolism ◽  
Papillary Muscles ◽  
O2 Consumption ◽  
Calcium Depletion ◽  
Experimental Conditions ◽  
High K

Basal metabolism has been measured in isolated whole hearts from rabbits and compared with myothermic and polarographic measurements on isolated papillary muscles. Hearts were perfused at constant pressure (Langendorff method) using a modified Krebs-Henseleit solution (KH) with glucose as substrate. Higher levels of basal O2 consumption (MVO2) and coronary flow (CF) were observed when arrest was induced by calcium depletion (low Ca; 0.1 mM CaCl2, 10.0 mM KCl) rather than by potassium excess (high K; 30.0 mM KCl). The metabolic rate of high K arrested hearts was close to earlier myothermic estimates (J. Mol. Cell. Cardiol. 16: 953-962, 1984); polarographic values, however, were about twofold higher, and somewhat higher than the value obtained in low Ca arrested hearts. The addition of erythrocytes, albumin, or dextran significantly reduced CF but did not substantially alter basal MVO2. Basal metabolic rate was substrate- and O2 tension-dependent, and under all experimental conditions there was linear relationship between MVO2 and CF. Extrapolations to zero flow showed that the basal MVO2 values so obtained were similar in low Ca or high K and were not altered by the presence of erythrocytes. Our results show that there are several factors regulating basal metabolism.

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