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Comparison of the Effects of Increased Myocardial Oxygen Consumption and Adenosine on the Coronary Microvascular Resistance
Journal article   Open access   Peer reviewed

Comparison of the Effects of Increased Myocardial Oxygen Consumption and Adenosine on the Coronary Microvascular Resistance

Hiroshi Kanatsuka, Kathryn Lamping, Charles Eastham, Kevin Dellsperger and Melvin Marcus
Circulation research, Vol.65(5), pp.1296-1305
11/1989
DOI: 10.1161/01.RES.65.5.1296
PMID: 2805245
url
https://doi.org/10.1161/01.RES.65.5.1296View
Published (Version of record) Open Access

Abstract

The purposes of this study were to determine if coronary dilation secondary to an increase in myocardial oxygen consumption (MVO2) affects the microcirculation in a homogeneous or heterogeneous manner and to determine if comparable degrees of coronary dilation produced by increasing MVO2 or exogenous (intravenous adenosine) or endogenous (intravenous dipyridamole) adenosine have similar effects In the coronary microcirculation. The epimyocardial coronary microcirculation was observed through an intravital microscope by stroboscopic epi-illumination in anesthetized open-chest dogs. Aortic pressure and heart rate were controlled by an aortic snare and atrioventricular sequential pacing, respectively, during experimental procedures. In group 1 (n = 15), coronary arterial microvessel diameters were measured under control condition and during rapid pacing at 300 beats/min, which doubled MVO2. Increases in MVO2 caused heterogeneous vasodilation in coronary arterial microvessels (40-380 μm). There was an inverse relation between control diameter and percent increase in diameter. In group 2 (n =15) or group 3 (n =10), adenosine or dipyridamole was infused intravenously to increase myocardial perfusion to the same level as that obtained with rapid pacing. Adenosine and dipyridamole did not change MVO2. Adenosine and dipyridamole also caused heterogeneous vasodilation, but the effects of adenosine and dipyridamole were restricted to arterial microvessels smaller than 150 μm. From these results, we conclude that increases in MVO2 produce widespread but heterogeneous vasodilation, that is, greater dilation in smaller arterial microvessels. Comparable increases in coronary flow produced by increasing MVO2 or endogenous and exogenous adenosine do not produce identical changes in the distribution of coronary microvascular resistance.

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