Increased coronary blood flow signals growth of coronary resistance vessels in near-term ovine fetuses

2002 ◽  
Vol 282 (1) ◽  
pp. R295-R302 ◽  
Author(s):  
D. Wothe ◽  
A. Hohimer ◽  
M. Morton ◽  
K. Thornburg ◽  
G. Giraud ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Fetal Sheep ◽  
Vascular Growth ◽  
Flow Reserve ◽  
Coronary Conductance ◽  
Near Term

We measured maximal coronary artery conductance in near-term fetal sheep before and after chronic infusion with adenosine to determine whether an increase in coronary flow without hypoxemia results in increased coronary vascular growth. Adenosine was infused into the circumflex coronary artery for 12 h each day for 4 days. Coronary flow was maintained at double the resting level by regulating the infusion of adenosine via a computerized servocontrol device signaled by a Doppler flow-velocity sensor. Total arterial hemoglobin, oxygen content, and hemodynamics were unchanged. Resting circumflex coronary blood flow increased from control of 250 ± 111 to 530 ± 216 ml · min−1 · 100 g left ventricle−1 with adenosine on day 1 and from 194 ± 74 to 878 ± 210 ml · min−1 · 100 g left ventricle−1 with adenosine on the last day ( P < 0.01). Coronary conductance, determined during maximal vasodilation, increased from 14.0 ± 5.0 to 26.9 ± 3.9 ml · min−1 · 100 g−1 · mmHg−1 over the 4 days ( P < 0.001). Coronary flow reserve, the difference between resting and maximal myocardial blood flow interpolated at 40 mmHg, increased from 299 ± 196 to 672 ± 266 ml · min−1 · 100 g−1( P < 0.001). Maximal coronary conductance was unchanged in control saline-infused fetuses (18.5 ± 5.1 vs. 18.5 ± 8.7 ml · min−1 · 100 g−1 · mmHg−1). We conclude that chronic intracoronary adenosine administration to the fetal myocardium modulates coronary vascular growth, even in the absence of tissue hypoxia.

Myocardial blood flow and coronary reserve in chronically anemic fetal lambs

1999 ◽  
Vol 277 (1) ◽  
pp. R306-R313 ◽  
Author(s):  
Lowell E. Davis ◽  
A. Roger Hohimer ◽  
Mark J. Morton
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Adenosine Infusion ◽  
Fetal Sheep ◽  
Coronary Reserve ◽  
Flow Reserve ◽  
Coronary Conductance ◽  
The Difference

Chronic fetal anemia produces large compensatory increases in coronary blood flow in the near-term fetal lamb. To determine if increased coronary flow in anemic fetuses is associated with decreased coronary flow reserve or, alternatively, an increase in coronary conductance, we measured maximal coronary artery conductance during adenosine infusion before and during anemia. Isovolemic hemorrhage over 7 days reduced hematocrit from 30.6 ± 2.7 to 15.8 ± 2.4% ( P < 0.02) and the oxygen content from 7.3 ± 1.4 to 2.6 ± 0.4 ml/dl ( P < 0.001). Coronary blood flow increased from control (202 ± 60) to 664 ± 208 ml ⋅ min−1 ⋅ 100 g−1 with adenosine to 726 ± 169 ml ⋅ min−1 ⋅ 100 g−1 during anemia and to 1,162 ± 250 ml ⋅ min−1 ⋅ 100 g−1 (left ventricle) during anemia with adenosine infusion (all P< 0.001). Coronary conductance, determined during maximal vasodilation, was 18.2 ± 7.7 before and 32.8 ± 11.9 ml ⋅ min−1 ⋅ 100 g−1 ⋅ mmHg−1during anemia ( P < 0.001). Coronary reserve, the difference between resting and maximal myocardial blood flow interpolated at 40 mmHg, was unchanged in control and anemic fetuses (368 ± 142 and 372 ± 201 ml/min). Because hematocrit affects viscosity, anemic fetuses were transfused with blood to acutely increase the hematocrit back to control, and conductance was remeasured. Coronary blood flow decreased 57.3 ± 18.9% but was still 42.6 ± 18.9% greater than control. We conclude that in chronically anemic fetal sheep coronary conductance is increased and coronary reserve is maintained, and this is attributed in part to angiogenesis as well as changes in viscosity.

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).

Role of K ATP + channels and adenosine in regulation of coronary blood flow in the hypertrophied left ventricle

1999 ◽  
Vol 277 (2) ◽  
pp. H617-H625 ◽  
Author(s):  
Peter J. Melchert ◽  
Dirk J. Duncker ◽  
Jay H. Traverse ◽  
Robert J. Bache
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Rate Pressure Product ◽  
Receptor Blockade ◽  
Channel Activity ◽  
Channel Blockade ◽  
Coronary Vasodilation ◽  
Exercise Induced

In the hypertrophied heart, increased extravascular forces acting to compress the intramural coronary vessels might require augmentation of metabolic vasodilator mechanisms to maintain adequate coronary blood flow. Vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity is important in metabolic coronary vasodilation, and adenosine contributes to resistance vessel dilation in the hypoperfused heart. Consequently, this study was performed to determine whether[Formula: see text] channels and adenosine have increased importance in exercise-induced coronary vasodilation in the hypertrophied left ventricle. Studies were performed in dogs in which banding of the ascending aorta had resulted in a 66% increase in left ventricular mass in comparison with historic normal animals. Treadmill exercise resulted in increases of coronary blood flow that were linearly related to the increase of heart rate or rate-pressure product. During resting conditions, [Formula: see text]channel blockade with glibenclamide caused a 17 ± 5% decrease in coronary blood flow, similar to that previously observed in normal hearts. Unlike normal hearts, however, glibenclamide blunted the increase in coronary flow that occurred during exercise, causing a significant decrease in the slope of the relationship between coronary flow and the rate-pressure product. Adenosine receptor blockade with 8-phenyltheophylline did not alter coronary blood flow at rest or during exercise. Furthermore, even after[Formula: see text] channel blockade with glibenclamide, the addition of 8-phenyltheophylline had no effect on coronary blood flow. This finding was different from normal hearts, in which the addition of adenosine receptor blockade after glibenclamide impaired exercise-induced coronary vasodilation. The data suggest that, in comparison with normal hearts, hypertrophied hearts have increased reliance on opening of [Formula: see text] channels to augment coronary flow during exercise. Contrary to the initial hypothesis, however, adenosine was not mandatory for exercise-induced coronary vasodilation in the hypertrophied hearts either during control conditions or when [Formula: see text] channel activity was blocked with glibenclamide.

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