scholarly journals Sympathetic control of major coronary artery diameter in the dog.

1979 ◽  
Vol 44 (4) ◽  
pp. 459-467 ◽  
Author(s):  
M Gerová ◽  
E Barta ◽  
J Gero
2013 ◽  
Vol 106 (8-9) ◽  
pp. 467
Author(s):  
F. Labombarda ◽  
G. Coutance ◽  
C. Mery ◽  
A. Hodzic ◽  
P. Dupont-Chauvet ◽  
...  

1992 ◽  
Vol 15 (11) ◽  
pp. 1711-1719 ◽  
Author(s):  
S. DEBORAH LUCY ◽  
DOUGLAS L. JONES ◽  
GEORGE J. KLEIN

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Maryse Lapierre-Landry ◽  
Hana Kolesová ◽  
Yehe Liu ◽  
Michiko Watanabe ◽  
Michael W. Jenkins

Abstract While major coronary artery development and pathologies affecting them have been extensively studied, understanding the development and organization of the coronary microvasculature beyond the earliest developmental stages requires new tools. Without techniques to image the coronary microvasculature over the whole heart, it is likely we are underestimating the microvasculature’s impact on normal development and diseases. We present a new imaging and analysis toolset to visualize the coronary microvasculature in intact embryonic hearts and quantify vessel organization. The fluorescent dyes DiI and DAPI were used to stain the coronary vasculature and cardiomyocyte nuclei in quail embryo hearts during rapid growth and morphogenesis of the left ventricular wall. Vessel and cardiomyocytes orientation were automatically extracted and quantified, and vessel density was calculated. The coronary microvasculature was found to follow the known helical organization of cardiomyocytes in the ventricular wall. Vessel density in the left ventricle did not change during and after compaction. This quantitative and automated approach will enable future cohort studies to understand the microvasculature’s role in diseases such as hypertrophic cardiomyopathy where misalignment of cardiomyocytes has been observed in utero.


1991 ◽  
Vol 17 (2) ◽  
pp. 338-345 ◽  
Author(s):  
Ken Okumura ◽  
Hirofumi Yasue ◽  
Koshi Matsuyama ◽  
Kozaburo Matsuyama ◽  
Yasuhiro Morikami ◽  
...  

1985 ◽  
Vol 249 (5) ◽  
pp. H981-H988 ◽  
Author(s):  
J. S. Schwartz ◽  
R. J. Bache

Previous studies have suggested that worsening hemodynamic severity of coronary stenoses in response to distal arteriolar dilation may be related to dilation of the normal epicardial artery adjacent to the stenosis resulting in increasing percent stenosis. To test this hypothesis we used sonomicrometry to continuously measure external circumflex coronary artery diameter distal to snare stenoses of varying severity in 19 open-chest dogs and 5 awake, chronically instrumented dogs. Arteriolar dilation produced by release of a transient coronary occlusion or by intracoronary injection of adenosine caused a decrease in circumflex coronary diameter distal to the stenosis. Regression analysis showed that circumflex diameter and pressure distal to the stenosis were directly related (mean r: transient occlusion, 0.86 +/- 0.04; adenosine, 0.97 +/- 0.01). The close relationship between pressure and diameter suggests that the decrease in diameter in response to arteriolar dilation was a passive effect. Passive coronary narrowing distal to a stenosis suggests that a similar effect may occur within a compliant stenosis, thus partly explaining the increase in severity of compliant stenoses in response to arteriolar dilation.


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