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Ann Thorac Surg 1990;50:323-329
© 1990 The Society of Thoracic Surgeons
Department of Surgery, Mercer University School of Medicine, and the Medical Center of Central Georgia, Macon, Georgia USA
* Address reprint requests to Dr Sealy, Department of Surgery, Hospital Box No. 140, The Medical Center of Central Georgia, 777 Hemlock St, Macon, GA 31208.
Correction of a coarctation of the aorta, an apparent simple cause of hypertension, paradoxically can provoke two hypertensive responses, one of which is potentially fatal. The first, limited to the first 24 hours, occurs in nearly one half of the patients. This is likely due to the high set of the carotid baroreceptors. The second, which may be associated with abdominal pain and, in some, with necrosis of the small bowel as a result of severe arteritis confined to arteries arising from the aorta below the coarctation, develops in about one half of the first responders. Norepinephrine excretion greatly increases for several days, whereas angiotensin levels are elevated for 3 to 4 days. The hypertension responds to β-blockers, to arterial smooth muscle relaxants, and to angiotensin converting enzymes. A theory is advanced to explain the second response. It is the adaptation gone awry that ensures adequate flow to exercising muscles below the coarctation, above and beyond that delivered by increasing the systolic pressure. It could be a regionally controlled mechanism similar to the rationing of blood flow in diving mammals.
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