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Research Article Free access | 10.1172/JCI109097
Cardiovascular Division, Department of Internal Medicine and Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242
Veterans Administration Hospital, Iowa City, Iowa 52242
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Cardiovascular Division, Department of Internal Medicine and Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242
Veterans Administration Hospital, Iowa City, Iowa 52242
Find articles by Marcus, M. in: JCI | PubMed | Google Scholar
Cardiovascular Division, Department of Internal Medicine and Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242
Veterans Administration Hospital, Iowa City, Iowa 52242
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Cardiovascular Division, Department of Internal Medicine and Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242
Veterans Administration Hospital, Iowa City, Iowa 52242
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Cardiovascular Division, Department of Internal Medicine and Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242
Veterans Administration Hospital, Iowa City, Iowa 52242
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Cardiovascular Division, Department of Internal Medicine and Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242
Veterans Administration Hospital, Iowa City, Iowa 52242
Find articles by Abboud, F. in: JCI | PubMed | Google Scholar
Published July 1, 1978 - More info
Morphologic observations suggest that the inner layers of the thoracic aorta in man and dog are avascular and the outer layers have vasa vasorum. It appears that vasa vasorum are essential in the thoracic aorta because their interruption produces medial necrosis. These experiments provide the first measurements of blood flow through aortic vasa vasorum and examine physiologic regulation of that flow.
During control conditions the outer two-thirds of the media of the thoracic aorta received 10 ml/min per 100 g blood flow through vasa vasorum. Flow to the inner third of the aorta was 1 ml/min per 100 g. Flow to both the inner and outer media of the abdominal aorta was less than 1 ml/min per 100 g. Adenosine increased blood flow to vasa vasorum in the outer media of the thoracic aorta from 7 to 18 ml/min per 100 g, but did not increase flow to the inner layers of the aorta. Hemorrhagic hypotension decreased flow in the outer media of the thoracic aorta from 14 to 2 ml/min per 100 g. Acute hypertension failed to increase blood flow through vasa vasorum, as conductance decreased significantly.
These studies indicate that vasa vasorum provide a considerable amount of blood flow to the outer layers of the thoracic aorta. The vessels are responsive to physiologic stimuli because they dilate during infusion of adenosine and constrict during both hemorrhagic hypotension and acute hypertension. We speculate that the failure of blood flow to the aortic wall to increase during acute hypertension might, if it were sustained, contribute to aortic medial necrosis.
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