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.

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.

Effect of coronary sinus occlusion on coronary pressure-flow relations

1980 ◽  
Vol 239 (1) ◽  
pp. H57-H64 ◽  
Author(s):  
R. F. Bellamy ◽  
H. S. Lowensohn ◽  
W. Ehrlich ◽  
R. W. Baer
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Sinus ◽  
Coronary Circulation ◽  
Reactive Hyperemia ◽  
Venous Pressure ◽  
Aortic Pressure ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
The Relationship

We studied the effect of transient occlusion of the coronary sinus on the relationship between aortic pressure and circumflex coronary blood flow in open-chest anesthetized dog preparations during artificially prolonged diastoles. The coronary pressure-flow relation was linear, and flow stopped at an arterial pressure (Pf = 0) that always exceeded coronary venous pressure (Pcv). During reactive hyperemia, Pf = 0 was 31 mmHg when Pcv was 5 mmHg and increased to 52 mmHg when the coronary sinus was occluded (Pcv, 38 mmHg). Elevation of Pcv translated the coronary pressure-flow relation to a higher Pf = 0 without altering the slope of the relation. Pf = 0 increased by about two-thirds of the increase in Pcv. We found no evidence that there existed a level of Pcv below which changes in Pcv had no effect on the coronary pressure-flow relation. These data are not compatible with the existence of a vascular waterfall mechanism in the coronary circulation unless it is assumed that Pcv is one of the determinants of Pf = 0.

Pulsatile Pressure and Flow in the Skeletal Muscle Microcirculation

1990 ◽  
Vol 112 (4) ◽  
pp. 437-443 ◽  
Author(s):  
Shou-Yan Lee ◽  
G. W. Schmid-Scho¨nbein
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Time Dependent ◽  
Physiological Importance ◽  
Pulsatile Pressure ◽  
Theoretical Predictions ◽  
Skeletal Muscle Microcirculation

Although blood flow in the microcirculation of the rat skeletal muscle has negligible inertia forces with very low Reynolds number and Womersley parameter, time-dependent pressure and flow variations can be observed. Such phenomena include, for example, arterial flow overshoot following a step arterial pressure, a gradual arterial pressure reduction for a step flow, or hysteresis between pressure and flow when a pulsatile pressure is applied. Arterial and venous flows do not follow the same time course during such transients. A theoretical analysis is presented for these phenomena using a microvessel with distensible viscoelastic walls and purely viscous flow subject to time variant arterial pressures. The results indicate that the vessel distensibility plays an important role in such time-dependent microvascular flow and the effects are of central physiological importance during normal muscle perfusion. In-vivo whole organ pressure-flow data in the dilated rat gracilis muscle agree in the time course with the theoretical predictions. Hemodynamic impedances of the skeletal muscle microcirculation are investigated for small arterial and venous pressure amplitudes superimposed on an initial steady flow and pressure drop along the vessel.

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.

Rat renal hemodynamics during venous compression: roles of nerves and prostaglandins

1985 ◽  
Vol 248 (6) ◽  
pp. F810-F820 ◽  
Author(s):  
A. Corradi ◽  
W. J. Arendshorst
Keyword(s):  
Arterial Pressure ◽  
Rat Kidney ◽  
Venous Pressure ◽  
General Pattern ◽  
Pressure Change ◽  
Renal Nerves ◽  
Venous Compression ◽  
Vasoactive Factors ◽  
Opposing Effects ◽  
Renal Vascular

Experiments were conducted on euvolemic rats to characterize renal hemodynamic responses to a unilateral increase in renal venous pressure. Ipsilateral renal blood flow (RBF, electromagnetic flow probe) was measured in four groups to determine the roles of the renal nerves and endogenous prostaglandins. In control rats, elevation of venous pressure (3 to 22 mmHg) produced vasoconstriction and a 16% increase in renal vascular resistance (RVR) at 130 mmHg arterial pressure (P less than 0.001). In acutely denervated kidneys, a 19-mmHg increase in venous pressure reduced RBF but did not alter RVR (5% decrease), since there were proportional decreases in RBF and the arteriovenous pressure gradient. Indomethacin-treated rats with innervated kidneys responded to a similar increase in venous pressure with pronounced constriction; RVR increased by 50% (P less than 0.005). Venous compression elicited a 24% increase in RVR (P less than 0.05) in indomethacin-treated rats with denervated kidneys. The opposing effects of denervation and indomethacin treatment were significant and noninteractive. The findings indicate 1) activation of an ipsilateral renorenal neural reflex mediated a significant portion of the vasoconstriction; and 2) enhanced synthesis of prostaglandins produced net dilatory effects that attenuated the neurally mediated constriction. The opposing actions of the renal nerves and prostaglandins on the RVR responses to increased venous pressure were directly related to arterial pressure between 70 and 130 mmHg. In response to decrements in arterial pressure, the general pattern of vasodilation was not impaired by denervation of indomethacin when venous pressure was normal or elevated. These observations indicate that the origin of the pressure change, i.e., arterial vs. venous, engages different vasoactive factors that are responsible for varying circulatory responses in the rat kidney.

Coronary sinus pressure and arterial flow during intermittent coronary sinus occlusion

1989 ◽  
Vol 256 (3) ◽  
pp. H906-H915
Author(s):  
F. Neumann ◽  
W. Mohl ◽  
W. Schreiner
Keyword(s):  
Coronary Sinus ◽  
Flow Curve ◽  
Methodological Approach ◽  
Venous Pressure ◽  
Artery Occlusion ◽  
Mean Value ◽  
Arterial Flow ◽  
The Mean ◽  
Release Ratio ◽  
Release Timing

The relationship between coronary artery flow and coronary venous pressure during intermittent coronary sinus occlusion was studied in dogs at normal perfusion, left anterior descending artery occlusion, and reperfusion. Coronary sinus occlusion and release phases were varied systematically. The periodicity of the data and the assumption of a linear relationship between pressure and flow suggested Fourier analysis as a methodological approach. To show the systematic slow oscillations of coronary venous pressure and arterial flow induced by intermittent occlusion of the coronary sinus, the data were smoothed by superimposing consecutive cycles of identical occlusion-release timing and filtering the higher frequencies. A small number of Fourier components, corresponding to the time scale of the respective occlusion-release cycle, was sufficient to study the long wavelength behavior. The effect of arbitrarily varying the occlusion-to-release ratio at a given total cycle length was investigated in hypothetical pressure and flow curves based on interpolation of experimental Fourier coefficients. By means of a transfer function relating pressure and flow in the frequency domain, it was possible to predict the arterial flow curve using coronary venous pressure measurements only. Because at zero frequency the pressure-flow relationship cannot be assumed to be linear, the mean value of flow could not be obtained in this way. However, the deviation of flow from the mean, i.e., the shape of the flow curve, was reproduced satisfactorily.

Blood volume restitution after hemorrhage in adult sheep

1987 ◽  
Vol 253 (4) ◽  
pp. R541-R544 ◽  
Author(s):  
J. M. Grimes ◽  
L. A. Buss ◽  
R. A. Brace
Keyword(s):  
Arterial Pressure ◽  
Experimental Evidence ◽  
Blood Volume ◽  
Plasma Protein ◽  
Time Course ◽  
Venous Pressure ◽  
Adult Sheep ◽  
Protein Mass ◽  
Female Sheep ◽  
Initial Blood

Indirect experimental evidence suggested the possibility that the restoration of blood volume to normal hemorrhage in adult sheep may occur more quickly than in other species that have been studied. To test this hypothesis, we studied unanesthetized chronically catheterized adult female sheep 1-2 wk after splenectomy. An average of 19.6 +/- 1.4% (SE) of their initial blood volume was removed over 10 min. Blood volume restitution at 0.5, 1, 3, 5, 7, 24, and 48 h posthemorrhage averaged 12 +/- 3, 34 +/- 3, 41 +/- 3, 50 +/- 4, 62 +/- 10, 79 +/- 10, and 124 +/- 25%, respectively. Arterial pressure decreased during the hemorrhage and returned to normal within 2 h, whereas venous pressure did not change significantly. No change in blood osmolality occurred. There was a highly significant correlation between blood volume and plasma protein mass (r = 0.98, P less than 10(-6)) during and after the hemorrhage. Thus it appears that the posthemorrhage restoration of blood volume in adult sheep occurs over essentially the same time course as in other species and this appears to be mediated by a restoration of plasma protein mass.

Changes in Coronary Artery Flow as Reaction to Coronary Sinus Occlusion

1984 ◽  
pp. 523-528 ◽  
Author(s):  
W. Mohl ◽  
A. Aigner ◽  
M. Moser ◽  
W. Timischl ◽  
R. Bauer
Keyword(s):  
Coronary Artery ◽  
Coronary Sinus ◽  
Coronary Artery Flow ◽  
Artery Flow

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.

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