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ORIGINAL ARTICLE |
Department of Cardiovascular and Thoracic Surgery, Showa University Tokyo, Japan
Masahiro Ohno, MD, Tel: +81 3 3784 8588, Fax: +81 3 3784 8307, Email: m.ohno21{at}med.showa-u.ac.jp, Department of Cardiovascular and Thoracic Surgery, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan.
ABSTRACT
Moderate hypothermic circulatory arrest with selective cerebral perfusion has been developed for cerebral protection during thoracic aortic surgery. However, visceral organs, particularly the kidneys, suffer greater tissue damage under moderate hypothermic circulatory arrest, and acute renal failure after hypothermic circulatory arrest is an independent risk factor for early and late mortality. This study investigated whether atrial natriuretic peptide could prevent the reduction in renal perfusion and protect renal function after moderate hypothermic circulatory arrest. Twelve pigs cooled to 30°C during cardiopulmonary bypass were randomly assigned to a peptide-treated group of 6 and a control group of 6. Moderate hypothermic circulatory arrest was induced for 60 min. Systemic arterial mean pressure and renal artery flow did not differ between groups during the study. However, renal medullary blood flow increased significantly in the peptide-treated group after hypothermic circulatory arrest. Myeloperoxidase activity was significantly reduced in the medulla of the peptide-treated group. Renal medullary ischemia after hypothermic circulatory arrest was ameliorated by atrial natriuretic peptide which increased medullary blood flow and reduced sodium reabsorption in the medulla. Atrial natriuretic peptide also reduced the release of an inflammatory marker after ischemia in renal tissue.
Key Words: Atrial Natriuretic Factor Heart Arrest Induced Hypothermia Induced Renal Circulation
Asian Cardiovasc Thorac Ann 2009;
17:401-407
© 2009 by SAGE Publications
DOI: 10.1177/0218492309341712
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