Preservation of coronary flow reserve in stunned myocardium

1989 ◽  
Vol 256 (5) ◽  
pp. H1303-H1310
Author(s):  
R. W. Jeremy ◽  
L. Stahl ◽  
M. Gillinov ◽  
M. Litt ◽  
T. R. Aversano ◽  
...  
Keyword(s):  
Coronary Flow Reserve ◽  
Coronary Flow ◽  
Coronary Occlusion ◽  
Myocardial Dysfunction ◽  
Reactive Hyperemia ◽  
Stunned Myocardium ◽  
Flow Reserve ◽  
Before And After ◽  
Adenosine Antagonist ◽  
Hyperemic Flow

Microvascular obstruction and persistent focal ischemia have been suggested as a possible cause of myocardial dysfunction (stunning) after brief coronary occlusion. Microvascular occlusion should result in a reduction in maximal coronary flow reserve, although resting transmural coronary flow may be maintained by release of local vasodilators, such as adenosine. To test the microvascular occlusion hypothesis, coronary flow reserve was measured in 14 anesthetized dogs, before and after myocardial stunning produced by 10 min of ischemia. Intracoronary adenosine infusion (5,900 microM/min) increased coronary flow to the same degree in normal [195 +/- 20 (SE) ml/min] and stunned (212 +/- 23 ml/min) myocardium. Peak hyperemic flow after 100 s of coronary occlusion was also similar in normal (205 +/- 25 ml/min) and stunned (218 +/- 23 ml/min) myocardium. The adenosine antagonist 8-phenyltheophylline (5 mg/kg) reduced the flow response to exogenous adenosine, but neither resting coronary flow nor peak hyperemic flow in stunned myocardium was altered. In stunned myocardium, myocardial shortening at rest (0.2 +/- 2.0%) increased during reactive hyperemia (to 13.8 +/- 2.5%, P less than 0.01), but shortening promptly returned to basal levels after each hyperemia. These findings indicate that fixed microvascular occlusion is unlikely to be an important factor in the pathogenesis of stunned myocardium and that local adenosine release does not appear to have a compensatory role in coronary vasoregulation in stunned myocardium.

Noninvasive Assessment of Coronary Flow Reserve Before and After Ranolazine Administration: Does It Improve in Our Real Patients?

2017 ◽  
Vol 5 (1) ◽  
Author(s):  
Pilar Egea-Serrano ◽  
Alfredo Vidal-Garcia ◽  
Salvador Montalban-Larrea ◽  
Ana I. Pelaez ◽  
Antonio Castilla
Keyword(s):  
Coronary Flow Reserve ◽  
Coronary Flow ◽  
Flow Reserve ◽  
Before And After ◽  
Noninvasive Assessment ◽  
Real Patients

Acute attenuation of glycocalyx barrier properties increases coronary blood volume independently of coronary flow reserve

2010 ◽  
Vol 298 (2) ◽  
pp. H515-H523 ◽  
Author(s):  
Judith Brands ◽  
Jos A. E. Spaan ◽  
Bernard M. Van den Berg ◽  
Hans Vink ◽  
Jurgen W. G. E. VanTeeffelen
Keyword(s):  
Red Blood Cells ◽  
Blood Volume ◽  
Coronary Flow Reserve ◽  
Blood Cells ◽  
Coronary Flow ◽  
Barrier Properties ◽  
Heart Tissue ◽  
Flow Reserve ◽  
Before And After ◽  
Coronary Conductance

Vascular endothelium is covered with an extensive mesh of glycocalyx constituents, which acts like an effective barrier up to several micrometers thick that shields the luminal surface of the vasculature from direct exposure to flowing blood. Many studies report that various enzymatic and pharmaceutical challenges are able to increase glycocalyx porosity, resulting in farther permeation of plasma macromolecules and greater access of red blood cells into glycocalyx domain. Attenuation of glycocalyx barrier properties therefore potentially increases the amount of blood that effectively occupies available microvascular volume. We tested in the present study whether attenuation of coronary glycocalyx barrier properties actually increases coronary blood volume and whether such changes would be noticeable during measurements of coronary flow reserve using adenosine. In anesthetized goats ( n = 6) with cannulated left main coronary artery that were perfused under controlled pressure, coronary blood volume was measured via the indicator-dilution technique using high-molecular-weight (2,000 kDa) dextrans as plasma tracer and labeled red blood cells as red blood cell tracer. Coronary blood volume was determined at baseline and during intracoronary infusion of adenosine causing maximal vasodilation (0.2–0.6 mg·kg−1·h−1) before and after intracoronary hyaluronidase treatment (170,000 units) of the glycocalyx. With an intact glycocalyx, coronary blood volume was 18.9 ± 1.1 ml/100 g heart tissue at baseline, which increased to 26.3 ± 2.7 ml/100 g after hyaluronidase treatment of the coronary glycocalyx. Maximal vasodilation by administration of adenosine further increased coronary blood volume to 33.9 ± 6.8 ml/100 g, a value not different from the maximal coronary blood volume of 33.2 ± 5.3 ml/100 g obtained by administration of adenosine in the absence of hyaluronidase treatment. Adenosine-induced increases in coronary conductance were not affected by hyaluronidase treatment. We conclude that acute attenuation of glycocalyx barrier properties increases coronary blood volume by ∼40%, which is of similar magnitude as additional changes in coronary blood volume during subsequent maximal vasodilation with adenosine. Furthermore, maximal coronary blood volume following administration of adenosine was similar with and without prior hyaluronidase degradation of the glycocalyx, suggesting that adenosine and hyaluronidase potentially increase glycocalyx porosity to a similar extent. Hyaluronidase-mediated changes in coronary blood volume did not affect baseline and adenosine-induced increases in coronary conductance, demonstrating that measurements of coronary flow reserve are insufficient to detect impairment of coronary blood volume recruitment in conditions of damaged glycocalyx.

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