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.

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.

Abstract 3628: Neuronal Nitric Oxide Synthase (nNOS) Regulates Basal Flow in the Human Coronary Circulation I n Vivo

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Mike Seddon ◽  
Phil Chowienczyk ◽  
Narbeh Melikian ◽  
Rafal Dworakowski ◽  
Barbara Casadei ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Coronary Flow ◽  
Vascular Tone ◽  
Coronary Circulation ◽  
Physiological Regulation ◽  
Intracoronary Doppler ◽  
Basal Flow

Endothelial NO synthase (eNOS) is thought to be the major source of nitric oxide (NO) involved in the local regulation of human vascular tone. However, in studies using a selective neuronal NOS (nNOS) inhibitor S-methyl-L-thiocitrulline (SMTC), we recently reported that basal human forearm blood flow is regulated by nNOS. SMTC had no effect on acetylcholine-induced vasodilatation which however was inhibited by the non-selective NOS inhibitor N G monomethyl-L-arginine (L-NMMA). This study investigated the effects of nNOS in the human coronary circulation in vivo . We studied patients undergoing diagnostic cardiac catheterisation who had angiographically normal coronary arteries. Coronary flow velocity was measured by an intracoronary Doppler wire and epicardial artery diameter by QCA. We compared the effects of intracoronary SMTC or L-NMMA infusion on basal flow and the responses to substance P and isosorbide dinitrate (endothelium-dependent and -independent dilators, respectively). L-NMMA (25 μmol/min) reduced basal coronary flow by 22.3±5.3% and inhibited dilation to substance P (20 pmol/min) by 57±5.7% (n=8; both P<0.01). SMTC (0.625 μmol/min) also reduced basal flow (−34.8±6.3%; n=8; P<0.01), but had no effect on the response to substance P (inhibited by −2±14%; P=NS). The effects of SMTC were abolished by L-arginine (240μmol/ min; n=3). Both L-NMMA and SMTC reduced epicardial artery diameter (−2.5±0.6% and −2.8±0.9% respectively; P<0.05) but only L-NMMA reduced dilatation to substance P (5.6±1.3% before versus 3.0±0.8% after L-NMMA; P<0.05). These data indicate that local nNOS-derived NO regulates basal coronary blood flow in humans in vivo , whereas substance P-stimulated vasodilatation is eNOS-mediated. Our results indicate that nNOS and eNOS have distinct local roles in the physiological regulation of human coronary vascular tone in vivo .

Quantification of O2 consumption and arterial pressure as independent determinants of coronary flow

1987 ◽  
Vol 252 (3) ◽  
pp. H545-H553 ◽  
Author(s):  
I. Vergroesen ◽  
M. I. Noble ◽  
P. A. Wieringa ◽  
J. A. Spaan
Keyword(s):  
Coronary Artery ◽  
Arterial Pressure ◽  
Coronary Flow ◽  
Left Main Coronary Artery ◽  
External Pressure ◽  
Arterial Blood Flow ◽  
O2 Consumption ◽  
Left Main ◽  
Arterial Blood ◽  
Wide Range

The steady-state relationship between coronary arterial blood flow (CBF) and both myocardial O2 consumption (MVO2) and coronary arterial pressure (P) was explored in anesthetized dogs and goats. Both species were subjected to constant pressure perfusion of the left main coronary artery by an external pressure-controlling circuit. In addition a group of goats was studied with normal aortic perfusion using an occluder around the left main coronary artery to vary coronary arterial pressure. The statistical analysis revealed that despite the direct effect of P on MVO2 (the Gregg effect) the effects of both variables on CBF were independent and linear over a wide range of P and MVO2 so that multiple regression analysis with a linear equation (CBF = a X P + b X MVO2 + c) gave an excellent fit which was not improved by the introduction of an addition interactive term b3MVO2 X P. The mean correlation coefficient for all animals was greater than 0.9. From these data we conclude that any factor regulating coronary arterial flow would be influenced by both MVO2 and perfusion pressure in an independent way. This study characterizes the stationary behavior of local coronary flow control. Hence, it specifies quantitatively the relations to be predicted by hypotheses aiming to explain this control mechanism.

Coronary sinus norepinephrine concentrations during ventricular tachycardia induced by left stellate ganglion stimulation in dogs

1988 ◽  
Vol 66 (4) ◽  
pp. 419-421 ◽  
Author(s):  
Réginald Nadeau ◽  
Daniel Lamontagne ◽  
René Cardinal ◽  
Jacques de Champlain ◽  
J. Andrew Armour
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Stellate Ganglion ◽  
Normal Myocardium ◽  
Sympathetic Stimulation ◽  
Sodium Thiopental ◽  
Cardiac Nerve ◽  
Left Stellate Ganglion ◽  
Ventricular Tachycardias

Coronary sinus catecholamine overflow was measured in open-chest dogs, anesthetized with sodium thiopental and α-chloralose, during left sympathetic stimulation. Uniform ventricular tachycardias were induced in 9 out of 16 dogs during either left stellate ganglion or left ventrolateral cardiac nerve stimulations. Significant increases in norepinephrine (8.1 ng/mL, plasma) and epinephrine (0.19 ng/mL, plasma) overflows were obtained after 30 and 90 s of stimulation, respectively. Maximum norepinephrine overflow was significantly higher in dogs with ventricular tachycardia than in those without it (16.0 vs. 7.4 ng/mL, p < 0.05). This suggests that the induction of ventricular tachycardia in the normal myocardium is related to the amount of local secretion of norepinephrine during nerve stimulation.

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.

Effect of Aortic Stenosis on Coronary Flow Dynamics: Studies in an In-Vitro Pulse Duplicating System

1982 ◽  
Vol 104 (3) ◽  
pp. 221-225 ◽  
Author(s):  
H. N. Sabbah ◽  
P. D. Stein
Keyword(s):  
Coronary Artery ◽  
Aortic Valve ◽  
Left Ventricle ◽  
Coronary Flow ◽  
Left Coronary Artery ◽  
Valvular Stenosis ◽  
Catheter Tip ◽  
Retrograde Coronary Flow

The dynamics of retrograde coronary flow in aortic valvular stenosis was investigated in an in-vitro pulse duplicating system which had the capability of simulating coronary flow. The ventricular chamber of the pulse duplicator consisted of an opaque elastic sac molded from rubber in the shape of a left ventricle. The aortic test section consisted of an acrylic mold of the root of the aorta of a calf, which included the sinuses of Valsalva and the entrance region of both the left and right coronary arteries. Flow in the left coronary artery was modeled to deliver both a systolic and a diastolic component of flow. Studies were performed with normal porcine valves in the aortic and mitral positions and were repeated with a human stenotic valve in the aortic position. Pressures were measured in the aorta, left ventricle, and at the ostium of the left coronary artery with catheter-tip micromanometers. In the presence of a normal aortic valve, total coronary flow was adjusted to 120 ml/min of which 21 percent of the flow occurred during systole. The phasic pattern of coronary flow was similar to that shown in vivo. In the presence of a stenotic aortic valve, a small amount of retrograde coronary flow (<1 percent of total coronary flow) was observed; and this occurred during the initial phase of systole. Retrograde coronary flow during systole appears to have resulted from compression of the collapsible segment of the simulated coronary artery. This was caused by the elevated simulated intramural pressure.

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.

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