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Research Article Free access | 10.1172/JCI105811
Robert Dawson Evans Memorial Department of Clinical Research, University Hospital, Boston University School of Medicine, Boston, Massachusetts 02118
Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118
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Robert Dawson Evans Memorial Department of Clinical Research, University Hospital, Boston University School of Medicine, Boston, Massachusetts 02118
Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118
Find articles by Kramsch, D. in: JCI | PubMed | Google Scholar
Robert Dawson Evans Memorial Department of Clinical Research, University Hospital, Boston University School of Medicine, Boston, Massachusetts 02118
Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118
Find articles by Farmelant, M. in: JCI | PubMed | Google Scholar
Robert Dawson Evans Memorial Department of Clinical Research, University Hospital, Boston University School of Medicine, Boston, Massachusetts 02118
Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118
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Published May 1, 1968 - More info
Coarctation of the mid-thoracic aorata was surgically produced in mongrel dogs which were sacrificed from 4-12 wk after the operation. As compared to the findings in control animals, the sodium, chloride, and water content of the hypetensive portion of the coarcted thoracic aorta was significantly elevated, whereas the electrolyte and water content of the relatively normotensive portion of the coarcted aorta was normal. The sodium, potassium, and water content of the pulmonary artery, skeletal muscle, and cardiac muscle of the coarcted dog was not altered. These observations suggest that an elevated arterial pressure may influence the electrolyte and water composition of the arteries.
The arterial pressure also may influence the content and synthesis of acid mucopolysaccharides (MPS) in the arteries since the content of sulfated MPS and the incorporation of injected radiosulfate into sulfated MPS were significantly increased in the hypertensive portion of the coarcted thoracic aorta but were significantly reduced in the relatively normotensive (“hypotensive”) portion of the coarcted aorta. The observed increase in MPS may have been a factor directly responsible for the increase in the sodium content of the hypertensive aorta since MPS can act as polyelectrolytes and bind cations.
Although the arterial pressure may influence certain metabolic functions in the arteries, it did not appear to have a direct effect on the arterial lipids since the lipid content of the hypertensive and of the relatively normotensive portions of the coarcted aorta were comparable to the values found in the normal aorta.
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