Original article
Direct effects of dobutamine on the coronary microcirculation: comparison with adenosine using myocardial contrast echocardiography☆

Presented in part at the 10th annual scientific sessions of the American Society of Echocardiography, Washington, DC, in May 1999.
https://doi.org/10.1067/S0894-7317(03)00423-1Get rights and content

Abstract

The direct effects of dobutamine on capillary blood volume (VOL) and blood flow velocity (VEL) are not known. We hypothesized that these would be more similar to that of adenosine because of its effects on the β2 receptors on the coronary circulation. A total of 9 open-chest anesthetized dogs were studied after placement of 2 noncritical stenoses at rest and during separate intracoronary administrations of 5 μg/kg−1/min−1 of adenosine and 2 μg/kg−1/min−1 of dobutamine. VOL and VEL were measured using myocardial contrast echocardiography, wall thickening with 2-dimensional echocardiography, and myocardial blood flow (MBF) with radiolabeled microspheres. Dobutamine increased the rate-pressure product significantly, whereas adenosine had no effect on the rate-pressure product. In the normal myocardium, adenosine had no effect on VOL and increases in MBF were all a result of increases in VEL. Dobutamine also caused mostly an increase in VEL and only a 30% increase in VOL indicating modest capillary recruitment. In the bed with stenosis both drugs attenuated increase in MBF by the same amount, which was associated with an attenuation in the increase in VEL secondary to a 15% increase in capillary resistance because of capillary derecruitment. The MBF-wall thickening relation was described for both drugs by the same function: y = 1 − exp(x) with wall thickening being significantly higher for dobutamine compared with adenosine for each level of MBF. We conclude that the increase in MBF in the normal myocardium with intracoronary dobutamine occurs mostly from an increase in VEL rather than from an increase in VOL. In the bed with a noncritical stenosis, the increases in MBF and VEL are similar for both drugs. Similar to intracoronary adenosine, intracoronary dobutamine also caused capillary derecruitment distal to a noncritical coronary stenosis.

Section snippets

Animal preparation

The study protocol was approved by our institutional animal research committee and conformed to the American Heart Association Guidelines for the Use of Animals in Research. A total of 9 adult, anesthetized, open-chest dogs, ventilated on room air, were used in this study. Catheters were placed in both femoral arteries for withdrawal of samples for blood gas and radiolabeled microsphere-derived MBF analysis, and in both femoral veins for infusion of fluids, drugs, and microbubbles. They were

Results

A total of 5 data sets were obtained in each dog: a resting stage and stages during dobutamine and adenosine for each of 2 levels of noncritical LAD stenosis. In 2 dogs only 1 stenosis was created. Table 1 depicts the hemodynamic data. Compared with both baseline and adenosine, dobutamine resulted in a significant increase in heart rate, rate-pressure product, and LCx CDP. Both drugs caused a similar increase in the mean gradient across the LAD stenosis without significantly changing the

Discussion

The new information in this study is that despite a greater increase in myocardial myocardial O2 consumption with intracoronary dobutamine, evidenced by the increase in both the rate-pressure product and WT, the increase in MBF in the normal myocardium occurred mostly from an increase in blood flow VEL rather than from an increase in MBV. In the bed with a noncritical stenosis, the increase in MBF and blood flow VEL was similar for both drugs. This is the first study to show that similar to

References (24)

  • S.G. Sawada et al.

    Echocardiographic detection of coronary artery disease during dobutamine infusion

    Circulation

    (1991)
  • R. Senior et al.

    Prognostic value of dobutamine stress echocardiography in patients undergoing diagnostic coronary arteriography

    Am J Cardiol

    (1997)
  • I. Afridi et al.

    Usefulness of isometric hand grip exercise in detecting coronary artery disease during dobutamine atropine stress echocardiography in patients with either stable angina pectoris or another type of positive stress test

    Am J Cardiol

    (1998)
  • S.C. Smart et al.

    Low-dose dobutamine echocardiography detects reversible dysfunction after thrombolytic therapy of acute myocardial infarction

    Circulation

    (1993)
  • R. Senior et al.

    Myocardial viability on echocardiography predicts long-term survival in patients with ischemic congestive heart failure

    J Am Coll Cardiol

    (1999)
  • J.L. Vanoverschelde et al.

    Hemodynamic and mechanical determinants of myocardial O2 consumption in normal human hearteffects of dobutamine

    Am J Physiol

    (1993)
  • J. Krivokapich et al.

    Dobutamine positron emission tomographyabsolute quantitation of rest and dobutamine myocardial blood flow and correlation with cardiac work and percent diameter stenosis in patients with and without coronary artery disease

    J Am Coll Cardiol

    (1996)
  • S.F. Vatner et al.

    Effects of dobutamine on left ventricular performance, coronary dynamics and distribution of cardiac output in conscious dogs

    J Clin Invest

    (1974)
  • K. Wei et al.

    Quantification of myocardial blood flow with ultrasound-induced destruction of microbubbles administered as a constant venous infusion

    Circulation

    (1998)
  • P. Eliason et al.

    Effect of intracoronary adenosine upon regional blood flow, microvascular volume, and hematocrit in the canine myocardium

    Int J Microcirc

    (1984)
  • J.P. Bin et al.

    Dobutamine versus dipyridamole for inducing reversible perfusion defects in chronic multivessel coronary artery stenosis

    J Am Coll Cardiol

    (2002)
  • L. Henquell et al.

    Intercapillary distances and capillary reserve in right and left ventriclessignificance for control of tissue PO2

    Microvasc Res

    (1976)

    • Cited by (0)

    ☆

    Supported in part by a grant (3R01-HL48890) from the National Institutes of Health, Bethesda, Md. Bristol Myers Squibb Medical Imaging, North Billerica, Mass, provided the radiolabeled microspheres; Phillips Ultrasound, Andover, Mass, provided the ultrasound system; and Amersham Health, Amersham, United Kingdom, provided the ultrasound contrast agent. Dr Le was supported by a postdoctoral training grant (HL-07355) from the National Institutes of Health. Dr Wei is the recipient of a Mentored Clinical Scientist Development Award (K08-HL03909) from the National Institutes of Health. Dr Coggins was the recipient of a medical student research grant from the American Diabetes Association, Washington DC.

    View full text
    Copyright © 2003 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.