The effect of vasoactive drugs on local coronary flow

1969 ◽  
Vol 47 (5) ◽  
pp. 421-425 ◽  
Author(s):  
Edilberto C. Torres ◽  
Giorgio Brandi
Keyword(s):  
Injection Site ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Coronary Vessels ◽  
Flow Volume ◽  
Vasoactive Drugs ◽  
Small Vessels ◽  
Receptor Sites ◽  
Xenon 133 ◽  
Selective Effects

A method is described by which it is possible to study the selective effects of vasoactive drugs on the small vessels of the coronary circulation of the dog. We incorporated xenon-133 with different drugs and derived the flow/volume ratios from the rate of fall of radioactivity at the injection site. Ratios were consistently reduced by angiotensin (−37%), pitressin (−40%), and propranolol (−13%), and were increased by dipyridamole (+23%), nitroglycerine (+14%), isoproterenol (+30%), adrenaline (+30%), and noradrenaline (+25%), indicating that these agents have an effect on the small coronary vessels. Ratios were unaltered by phenylephrine and by combinations of propranolol with adrenaline or noradrenaline, suggesting that alpha receptor sites may be absent from the small vessel bed under study.

scholarly journals Coronary flow in a perfused rainbow trout heart

1987 ◽  
Vol 129 (1) ◽  
pp. 107-123 ◽  
Author(s):  
A. P. Farrell
Keyword(s):  
Rainbow Trout ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Coronary Vessels ◽  
Cardiac Metabolism ◽  
Salmo Gairdneri ◽  
Acclimation Temperature ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Temperature Dependent

A preparation was developed to perfuse the coronary circulation in working hearts from rainbow trout (Salmo gairdneri Richardson). The preparation was used to examine pressure-flow relationships for the coronary circulation as the heart generated physiological and subphysiological work loads. Coronary vascular resistance increased exponentially as coronary flow rate decreased. Coronary resistance was also influenced by cardiac metabolism and acclimation temperature. When heart rate was increased, extravascular compression increased in coronary resistance. Direct vasoconstriction of the coronary vessels, produced by injections of adrenaline into the coronary circulation, was temperature-dependent.

Coronary vasomotor tonus in atherosclerotic dogs

1962 ◽  
Vol 202 (4) ◽  
pp. 616-618 ◽  
Author(s):  
Cecil E. Cross ◽  
Robert W. Oblath
Keyword(s):  
Coronary Arteries ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Heart Weight ◽  
Propulsive Force ◽  
Vasoactive Drugs

The atherogenic regimen imposed upon the animals studied here resulted in several distinct abnormalities of the coronary circulation. The structure of the coronary arteries was modified by extensive atheromatous deposits. During control states before the administration of vasoactive drugs, coronary flow per unit of net propulsive force and heart weight was unvaried or increased. The ability of the atheromatous coronary tree to increase or decrease its vasomotor tonus was markedly curtailed. The abnormalities mentioned here were proportional with the severity of the atherogenic regimen.

Flow-volume relations in coronary circulation and distribution of coronary flow into nutritional and non-nutritional compartments

1983 ◽  
Vol 3 (4) ◽  
pp. 349-357 ◽  
Author(s):  
Kari S. Virtanen ◽  
Antero Järvinen ◽  
Ilkka Alitalo ◽  
Esko Riihimäki
Keyword(s):  
Coronary Flow ◽  
Coronary Circulation ◽  
Flow Volume

scholarly journals THE INFLUENCE OF EPINEPHRIN UPON THE CORONARY CIRCULATION OF THE MONKEY

1915 ◽  
Vol 21 (4) ◽  
pp. 330-336 ◽  
Author(s):  
Henry G. Barbour ◽  
Alexander L. Prince
Keyword(s):  
Coronary Arteries ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Coronary Vessels ◽  
Locke Solution

Decrease in coronary flow was the constant response of freshly isolated monkey hearts to epinephrin. These hearts were perfused with autogenous hirudinized blood diluted with Locke solution. The results were constant at high or low perfusion pressures, in beating or resting hearts, and with all adequate doses. Increased coronary flow was obtained constantly in rabbit hearts under identical conditions. In the light of previous work upon isolated human coronary arteries, the general conclusion is drawn that, while actively dilating the coronary vessels in the dog, cat, rabbit, ox, sheep, and pig, epinephrin constricts the coronary vessels in man and the monkey. The coronary arteries of the last two species are presumably supplied with constrictor nerves of true sympathetic (thoracicolumbar) origin.

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 .

Nitric oxide modulates epicardial coronary basal vasomotor tone in awake dogs

1990 ◽  
Vol 258 (4) ◽  
pp. H1250-H1254 ◽  
Author(s):  
A. Chu ◽  
D. E. Chambers ◽  
C. C. Lin ◽  
W. D. Kuehl ◽  
F. R. Cobb
Keyword(s):  
Nitric Oxide ◽  
Coronary Flow ◽  
Diastolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Vasomotor Tone ◽  
Coronary Vasomotor Tone ◽  
Endogenous Nitric Oxide

This study evaluates the role of endogenous nitric oxide in the modulation of basal coronary vasomotor tone by studying the effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide formation from L-arginine, on resting epicardial coronary diameter and coronary flow. L-NMMA (5 mg/kg) was infused in seven awake dogs chronically instrumented with coronary dimension crystals for measurement of epicardial coronary diameter, and Doppler flow probes for quantitation of phasic coronary flow (vasomotion of distal regulatory resistance coronary vessels). Epicardial coronary diameter decreased 5.5% from 3.47 +/- 0.17 to 3.28 +/- 0.15 mm (mean +/- SE). The diameter change was gradual, reaching a maximum at 13 +/- 2 min after infusion, and persistent, lasting greater than 90 min. Phasic coronary flow did not change. Mean aortic pressure significantly increased from 99 +/- 3 to 111 +/- 3 mmHg and heart rate decreased from 56 +/- 4 to 46 +/- 3 beats/min. Left ventricular end-diastolic pressure and contractility were not significantly altered. L-Arginine (66 mg/kg) but not D-arginine reversed all hemodynamic parameters. These data support an important role of nitric oxide in modulating basal epicardial coronary vasomotor tone and systemic vascular resistance.

Bifurcation asymmetry of the porcine coronary vasculature and its implications on coronary flow heterogeneity

2004 ◽  
Vol 287 (6) ◽  
pp. H2493-H2500 ◽  
Author(s):  
Ghada Kalsho ◽  
Ghassan S. Kassab
Keyword(s):  
Blood Flow ◽  
Coronary Vessels ◽  
Significant Heterogeneity ◽  
Branching Pattern ◽  
Optical Sectioning ◽  
Coronary Vasculature ◽  
Coronary Veins ◽  
Flow Heterogeneity ◽  
Small Vessels ◽  
Arteries And Veins

The branching pattern of the coronary arteries and veins is asymmetric, i.e., many small vessels branch off of a large trunk such that the two daughter vessels at a bifurcation are of unequal diameters and lengths. One important implication of the geometric vascular asymmetry is the dispersion of blood flow at a bifurcation, which leads to large spatial heterogeneity of myocardial blood flow. To document the asymmetric branching pattern of the coronary vessels, we computed an asymmetry ratio for the diameters and lengths of all vessels, defined as the ratio of the daughter diameters and lengths, respectively. Previous data from silicone elastomer cast of the entire coronary vasculature including arteries, arterioles, venules, and veins were analyzed. Data on smaller vessels were obtained from histological specimens by optical sectioning, whereas data on larger vessels were obtained from vascular casts. Asymmetry ratios for vascular areas, volumes, resistances, and flows of the various daughter vessels were computed from the asymmetry ratios of diameters and lengths for every order of mother vessel. The results show that the largest orders of arterial and venous vessels are most asymmetric and the degree of asymmetry decreases toward the smaller vessels. Furthermore, the diameter asymmetry at a bifurcation is significantly larger for the coronary veins (1.7–6.8 for sinus veins) than the corresponding arteries (1.5–5.8 for left anterior descending coronary artery) for orders 2–10, respectively. The reported diameter asymmetry at a bifurcation leads to significant heterogeneity of blood flow at a bifurcation. Hence, the present data quantify the dispersion of blood flow at a bifurcation and are essential for understanding flow heterogeneity in the coronary circulation.

In vivo measurement of coronary circulation angiotensin-converting enzyme activity in humans

2003 ◽  
Vol 284 (1) ◽  
pp. H17-H22 ◽  
Author(s):  
Cezar Staniloae ◽  
Andreas J. Schwab ◽  
André Simard ◽  
Richard Gallo ◽  
Ihor Dyrda ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Coronary Circulation ◽  
Coronary Vessels ◽  
Capillary Endothelium ◽  
Converting Enzyme ◽  
In Vivo Measurement ◽  
Atherosclerotic Burden ◽  
Wide Range ◽  
Ace Activity

Angiotensin-converting enzyme (ACE) is present on the luminal surface of the coronary vessels, mostly on capillary endothelium. ACE is also expressed on coronary smooth muscle cells and on plaque lipid-laden macrophages. Excessive coronary circulation (CC)-ACE activity might be linked to plaque progression. Here we used the biologically inactive ACE substrate3H-labeled benzoyl-Phe-Ala-Pro ([3H]BPAP) to quantify CC-ACE activity in 10 patients by means of the indicator-dilution technique. The results were compared with atherosclerotic burden determined by coronary angiography. There was a wide range of CC-ACE activity as revealed by percent [3H]BPAP hydrolysis (30–74%). The atherosclerotic extent scores ranged from 0.0 to 66.97, and the plaque area scores ranged from 0 to 80 mm2. CC-ACE activity per unit extracellular space ( V max/ K m V i), an index of metabolically active vascular surface area, was correlated with myocardial blood flow ( r = 0.738; P = 0.03) but not with measures of the atherosclerotic burden. These results show that CC-ACE activity can be safely measured in humans and that it is a good marker of the vascular area of the perfused myocardium. It does not, however, reflect epicardial atherosclerotic burden, suggesting that local tissue ACE may be more important in plaque development.

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