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Research Article Free access | 10.1172/JCI114053

Regional atrial blood flow in dogs. Effect of hypertrophy on coronary flow reserve.

R P Bauman, J C Rembert, and J C Greenfield Jr

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.

Find articles by Bauman, R. in: PubMed | Google Scholar

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.

Find articles by Rembert, J. in: PubMed | Google Scholar

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.

Find articles by Greenfield, J. in: PubMed | Google Scholar

Published May 1, 1989 - More info

Published in Volume 83, Issue 5 on May 1, 1989
J Clin Invest. 1989;83(5):1563–1569. https://doi.org/10.1172/JCI114053.
© 1989 The American Society for Clinical Investigation
Published May 1, 1989 - Version history
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Abstract

Little is known regarding regional atrial blood flow responses during varying hemodynamic states in both the normal and hypertrophied atria. This study was undertaken to develop a canine model of chronic atrial hypertrophy and to define in both this group and in normal dogs the regional blood flow response to acute atrial fibrillation and to measure coronary flow reserve. In the 12 dogs with atrial but not ventricular hypertrophy the mean left and right atrial weights were 75 and 47% respectively greater than in the normal group. Blood flow in the normal dogs was less in the appendage than in the non-appendage region for both atria and increased significantly during atrial fibrillation. Similar findings were noted in the hypertrophy group except that during control conditions the left atrial appendage flow was similar to the nonappendage flow. Minimal vascular resistance for the hypertrophy group, 39 +/- 3 was significantly (P less than 0.05) greater when compared to the normal group 28 +/- 2 mmHg/cm3 per min per g. Thus, significant regional blood flow differences occur in both the normal and hypertrophied atria. In addition, atrial hypertrophy does not alter the autoregulatory capacity to the hemodynamic stress of atrial fibrillation but does reduce coronary flow reserve.

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