Modulation of coronary flow by left ventricular volume in the presence and absence of vasomotor tone

D. Manor, S. Williams, R. Ator, K. Bryant and K. W. Scheel Department of Physiology, University of North Texas Health Science Center at Fort Worth 76101-2699, USA. This study was undertaken to determine the relationship between left ventricular (LV) volume and coronary flow in the presence and absen...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 1995-12, Vol.269 (6), p.H2010-H2016
Hauptverfasser: Manor, D, Williams, S, Ator, R, Bryant, K, Scheel, K. W
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Sprache:eng
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Zusammenfassung:D. Manor, S. Williams, R. Ator, K. Bryant and K. W. Scheel Department of Physiology, University of North Texas Health Science Center at Fort Worth 76101-2699, USA. This study was undertaken to determine the relationship between left ventricular (LV) volume and coronary flow in the presence and absence of coronary vasomotor tone in arrested dog hearts. We utilized an isolated, blood-perfused, potassium-arrested dog heart preparation with vascular vasomotor tone present (n = 5) or after maximal vasodilation with adenosine (n = 7). LV volume was controlled with a balloon while left and right coronary flows were recorded. Left and right coronary flows were plotted as a function of LV volume, and the degree of interdependency was quantitatively assessed by the slope of the linear regression and the correlation coefficient (r) between coronary flow and LV volume. With vasomotor tone present, both left (slope = 0.01 +/- 0.06 min-1) and right (slope = -0.01 +/- 0.01 min-1) coronary arterial flows were maintained relatively constant over a wide range of LV volumes. After maximal vasodilation, left coronary flow decreased linearly with LV volume loading (slope = -2.51 +/- 0.47 min-1, r2 = 0.96 +/- 0.02), whereas right coronary flow, similar to the response with tone present, did not change relative to control in most cases. We conclude that changes in coronary vasomotor tone may take place with LV volume loading to compensate for the mechanical vascular resistance changes secondary to myocardial stretch.
ISSN:0363-6135
0002-9513
1522-1539
DOI:10.1152/ajpheart.1995.269.6.H2010