Role of site of microsphere injection and catheter position on systemic and regional hemodynamics in rat

1984 ◽  
Vol 247 (1) ◽  
pp. H35-H39 ◽  
Author(s):  
I. Kobrin ◽  
M. B. Kardon ◽  
W. Oigman ◽  
B. L. Pegram ◽  
E. D. Frohlich
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Ventricular Catheter ◽  
Catheter Position ◽  
Flow Measurements ◽  
Conscious Rats ◽  
Anesthetized Rats ◽  
Regional Hemodynamics

The influences of the site of microsphere injection (intra-atrial vs. intraventricular) and positioning of the left ventricular catheter (aortoventricular vs. atrioventricular) on systemic, renal, and coronary hemodynamics were evaluated in anesthetized rats. The effect of anesthesia on aortoventricular catheter positioning was also evaluated. In anesthetized and open-chest preparations, the systemic and renal hemodynamics were not affected by catheter position or site of microsphere injection; however, myocardial blood flow was dependent on these variables. Variations in coronary blood flow were significantly greater when the catheter was in the aortoventricular position (34 +/- 3%) than with an atrioventricular catheter (11 +/- 2%, P less than 0.01), irrespective of whether the microspheres were injected into the atrium or ventricle. Comparison of anesthetized and conscious rats with aortoventricular catheter indicated lesser variability in coronary blood flow in the conscious rats (P less than 0.01). Therefore, the greater variability of coronary flow measurements in anesthetized rats was caused by the position of the cardiac catheter in the aortoventricular route. However, the variability caused by the aortoventricular catheter was much less in conscious rats. Therefore, coronary flow hemodynamic measurements (microsphere technique) are less variable when they are made in conscious rats.

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.

Regulation of coronary flow

2021 ◽  
pp. 11-13
Author(s):  
Nico Bruining ◽  
Eric Boersma ◽  
Dirk J. Duncker
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Arterial Blood ◽  
Arterial Inflow ◽  
Systolic Phase ◽  
Vascular Beds

This chapter describes the regulation of coronary blood flow. The left ventricle generates the systemic arterial blood pressure that is required to maintain coronary blood flow. The coronary circulation is unique among regional vascular beds in that its perfusion is impeded during the systolic phase of the cardiac cycle by the surrounding contracting cardiac muscle. Systolic contraction increases left ventricular wall tension and compresses the intramyocardial microvessels, thereby impeding coronary arterial inflow. This compression is not uniformly distributed across the left ventricular wall, resulting in a redistribution of blood flow from the subendocardium to subepicardium.

Intramyocardial Pressure and Coronary Extravascular Resistance

1985 ◽  
Vol 107 (1) ◽  
pp. 46-50 ◽  
Author(s):  
P. D. Stein ◽  
H. N. Sabbah ◽  
M. Marzilli
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Driving Pressure ◽  
Ventricular Pressure ◽  
Intramyocardial Pressure ◽  
Extravascular Resistance

Intramyocardial pressure is an indicator of coronary extravascular resistance. During systole, pressure in the subendocardium exceeds left ventricular intracavitary pressure; whereas pressure in the subepicardium is lower than left ventricular intracavitary pressure. Conversely, during diastole, subepicardial pressure exceeds both subendocardial pressure and left ventricular pressure. These observations suggest that coronary flow during systole is possible only in the subepicardial layers. During diastole, however, a greater driving pressure is available for perfusion of the subendocardial layers relative to the subepicardial layers. On this basis, measurements of intramyocardial pressure contribute to an understanding of the mechanisms of regulation of the phasic and transmural distribution of coronary blood flow.

Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion

1985 ◽  
Vol 249 (6) ◽  
pp. H1070-H1077 ◽  
Author(s):  
I. Y. Liang ◽  
C. E. Jones
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Adrenergic Blockade ◽  
Adrenergic Antagonist

Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6–8 min of prazosin infusion (0.6–0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.

Alpha 1-adrenergic constriction limits coronary flow and cardiac function in running dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1117-H1126 ◽  
Author(s):  
P. A. Gwirtz ◽  
S. P. Overn ◽  
H. J. Mass ◽  
C. E. Jones
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Receptor Blocker ◽  
Adrenergic Blockade

Modulation of coronary blood flow and cardiac function by alpha 1-adrenergic receptors was examined in dogs during strenuous exercise. Fifteen dogs were chronically instrumented to measure left circumflex blood flow, heart rate, regional left ventricular function (systolic shortening, and rate of shortening), and global left ventricular function (left ventricular pressure, and dP/dt). The specific postsynaptic alpha 1-receptor blocker prazosin (0.5 mg) and nonselective alpha-receptor blocker phentolamine (1.0 mg) were injected through an indwelling circumflex artery catheter to produce local adrenergic blockade of the posterior left ventricular region during exercise. Exercise significantly increased heart rate, left ventricular systolic pressure, dP/dt, segment shortening and rate of shortening, and coronary blood flow. Both prazosin and phentolamine caused similar additional increases in dP/dt by 21 +/- 4%, in rate of shortening in the posterior region by 37 +/- 6%, and in myocardial O2 consumption by 26 +/- 11%, which were associated with a 21 +/- 3% increase in coronary flow during exercise but no change in O2 extraction. Similar results were obtained when dogs were beta-blocked with either atenolol (1.0 mg ic) or propranolol (1.0 mg ic) prior to exercise. These data suggest that an alpha 1-vasoconstriction modulates O2 delivery to myocardial tissue and limits both coronary vasodilation and cardiac function during exercise.

Effects of Elevated Coronary Sinus Pressure on Coronary Blood Flow and Left Ventricular Function

Circulation ◽  
1995 ◽  
Vol 92 (9) ◽  
pp. 298-303 ◽  
Author(s):  
Takuya Miura ◽  
Takeshi Hiramatsu ◽  
Joseph M. Forbess ◽  
John E. Mayer
Keyword(s):  
Blood Flow ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Left Ventricular ◽  
Sinus Pressure

alpha-Adrenergic control of oxygen delivery to myocardium during exercise in conscious dogs

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Oxygen Delivery ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Adrenergic Control

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.

Alteration in myocardial oxygen balance during exercise after beta-adrenergic blockade in dogs

1980 ◽  
Vol 49 (1) ◽  
pp. 28-33 ◽  
Author(s):  
G. R. Heyndrickx ◽  
J. L. Pannier ◽  
P. Muylaert ◽  
C. Mabilde ◽  
I. Leusen
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Oxygen Balance

The effects of beta-adrenergic blockade upon myocardial blood flow and oxygen balance during exercise were evaluated in eight conscious dogs, instrumented for chronic measurements of coronary blood flow, left ventricular pressure, aortic blood pressure, heart rate, and sampling of arterial and coronary sinus venous blood. The administration of propranolol (1.5 mg/kg iv) produced a decrease in heart rate, peak left ventricular (LV) dP/dt, LV (dP/dt/P, and an increase in LV end-diastolic pressure during exercise. Mean coronary blood flow and myocardial oxygen consumption were lower after propranolol than at the same exercise intensity in control conditions. The oxygen delivery-to-oxygen consumption ratio and the coronary sinus oxygen content were also significantly lower. It is concluded that the relationship between myocardial oxygen supply and demand is modified during exercise after propranolol, so that a given level of myocardial oxygen consumption is achieved with a proportionally lower myocardial blood flow and a higher oxygen extraction.

Computer Analysis of Coronary Doppler Flow Velocity

2008 ◽  
pp. 281-289
Author(s):  
Valentina Magagnin ◽  
Maurizio Turiel ◽  
Sergio Cerutti ◽  
Luigi Delfino ◽  
Enrico Caiani
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Flow Velocity ◽  
Coronary Blood Flow ◽  
Doppler Echocardiography ◽  
Coronary Flow ◽  
Connective Tissue Diseases ◽  
Doppler Flow ◽  
Intracoronary Doppler ◽  
Artery Disease

The coronary flow reserve (CFR) represents an important functional parameter to assess epicardial coronary stenosis and to evaluate the integrity of coronary microcirculation (Kern, 2000; Sadamatsu, Tashiro, Maehira, & Yamamoto, 2000). CFR can be measured, during adenosine or dipyridamole infusion, as the ratio of maximal (pharmacologically stimulated) to baseline (resting) diastolic coronary blood flow peak. Even in absence of stenosis in epicardial coronary artery, the CFR may be decreased when coronary microvascular circulation is compromised by arterial hypertension with or without left ventricular hypertrophy, diabetes mellitus, hypercholesterolemia, syndrome X, hypertrophic cardiomyopathy, and connective tissue diseases (Dimitrow, 2003; Strauer, Motz, Vogt, & Schwartzkopff, 1997). Several methods have been established for measuring CFR: invasive (intracoronary Doppler flow wire) (Caiati, Montaldo, Zedda, Bina, & Iliceto, 1999b; Lethen, Tries, Brechtken, Kersting, & Lambertz, 2003a; Lethen, Tries, Kersting, & Lambertz, 2003b), semi-invasive and scarcely feasible (transesophageal Doppler echocardiography) (Hirabayashi, Morita, Mizushige, Yamada, Ohmori, & Tanimoto, 1991; Iliceto, Marangelli, Memmola, & Rizzon, 1991; Lethen, Tries, Michel, & Lambertz, 2002; Redberg, Sobol, Chou, Malloy, Kumar, & Botvinick, 1995), or extremely expensive and scarcely available methods (PET, SPECT, MRI) (Caiati, Cioglia, Montaldo, Zedda, Rubini, & Pirisi, 1999a; Daimon, Watanabe, Yamagishi, Muro, Akioka, & Hirata, 2001; Koskenvuo, Saraste, Niemi, Knuuti, Sakuma, & Toikka, 2003; Laubenbacher, Rothley, Sitomer, Beanlands, Sawada, & Sutor, 1993; Picano, Parodi, Lattanzi, Sambuceti, Andrade, & Marzullo, 1994; Saraste, Koskenvuo, Knuuti, Toikka, Laine, & Niemi, 2001; Williams, Mullani, Jansen, & Anderson, 1994), thus their clinical use is limited (Dimitrow, 2003). In addition, PET and intracoronary Doppler flow wire involve radiation exposure, with inherent risk, environmental impact, and biohazard connected with use of ionizing testing (Picano, 2003a). In the last decade, the development of new ultrasound equipments and probes has made possible the noninvasive evaluation of coronary blood velocity by Doppler echocardiography, using a transthoracic approach. In this way, the peak diastolic coronary flow velocity reserve (CFVR) can be estimated as the ratio of the maximal (pharmacologically stimulated) to baseline (resting) diastolic coronary blood flow velocity peak measured from the Doppler tracings. Several studies have shown that peak diastolic CFVR, computed in the distal portion of the left anterior descending (LAD) coronary artery, correlates with CFR obtained by more invasive techniques. This provided a reliable and non invasive tool for the diagnosis of LAD coronary artery disease (Caiati et al., 1999b; Caiati, Montaldo, Zedda, Montisci, Ruscazio, & Lai, 1999c; Hozumi, Yoshida, Akasaka, Asami, Ogata, & Takagi, 1998; Koskenvuo et al., 2003; Saraste et al., 2001).

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