HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Stephan Thelitz Frank L. Hanley Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Malhotra, S. P. Articles by Riemer, R. K. Search for Related Content PubMed PubMed Citation Articles by Malhotra, S. P. Articles by Riemer, R. K. Related Collections Congenital - cyanotic

J Thorac Cardiovasc Surg 2002;123:655-660
© 2002 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease (CHD)

Cavopulmonary anastomosis induces pulmonary expression of the angiotensin II receptor family

From the Division of Cardiothoracic Surgery, University of California, San Francisco, Calif.

Presented at the 73rd Annual Scientific Sessions of the American Heart Association, New Orleans, La, Nov 14, 2000.

Received for publication April 24, 2001. Revisions requested June 13, 2001; revisions received Aug 7, 2001. Accepted for publication Aug 20, 2001. Address for reprints: R. Kirk Riemer, PhD, Department of Cardiothoracic Surgery, Stanford University, Falk Cardiovascular Research Center, 300 Pasteur Dr, Stanford, CA 94305-5407 (E-mail: riemerk{at}surgery.ucsf.edu).

Background: Cavopulmonary anastomosis is used for palliation of cyanotic cardiac lesions. Postoperative development of pulmonary arteriovenous malformations can be significant in 10% to 25% of patients. To study the basis for formation of arteriovenous malformations, we developed an ovine model that reliably induces their development 8 weeks after cavopulmonary anastomosis. Previously, we found that cavopulmonary anastomosis inhibits the expression of pulmonary angiotensin-converting enzyme and suppresses angiotensin II production.
Objective: This study examines the role of the angiotensin II receptors, type 1 and type 2, in this setting of pulmonary vascular remodeling.
Methods: Lambs, aged 40 to 50 days, underwent cavopulmonary anastomosis. In age-matched control animals, a sham operation was performed. Messenger RNA and protein expression in lung specimens was measured at successive time points after cavopulmonary anastomosis or sham operations (n = 3 at each time point).
Results: Angiotensin type 1 mRNA was maximally upregulated 2-fold at 5 weeks after cavopulmonary anastomosis (P = .006). Expression of angiotensin type 1 protein was increased at least 2-fold at 2, 5, and 15 weeks after cavopulmonary anastomosis (P = .005). Cavopulmonary anastomosis also increased angiotensin type 2 mRNA and protein expression at least 2-fold at 2 and 5 weeks (P = .02) after surgical intervention. At 15 weeks, expression of angiotensin type 2 mRNA and protein was unchanged from that seen in control animals. Immunolocalization in pulmonary tissue sections 2 weeks after cavopulmonary anastomosis revealed markedly enhanced staining of angiotensin II receptor type 1 in vascular smooth muscle and angiotensin II receptor type 2 in the endothelium of pulmonary arteries.
Conclusions: Rapid elevation in the expression of the type 1 and 2 angiotensin II receptors in the affected pulmonary vasculature after cavopulmonary anastomosis suggests their involvement in the pathologic vascular remodeling that occurs after cavopulmonary anastomosis.

This article has been cited by other articles:

				D. Miniati, E. B. Jelin, J. Ng, J. Wu, T. R. Carlson, X. Wu, M. R. Looney, and R. A. Wang Constitutively active endothelial Notch4 causes lung arteriovenous shunts in mice Am J Physiol Lung Cell Mol Physiol, February 1, 2010; 298(2): L169 - L177. [Abstract] [Full Text] [PDF]

				E. J. Hickey, A. A. Alghamdi, M. Elmi, K. S. Al-Najashi, G. S. Van Arsdell, C. A. Caldarone, J. Coles, and W. G. Williams Systemic arteriovenous fistulae for end-stage cyanosis after cavopulmonary connection: A useful bridge to transplantation J. Thorac. Cardiovasc. Surg., January 1, 2010; 139(1): 128 - 134. [Abstract] [Full Text] [PDF]

				D. B. McElhinney, J. Kreutzer, P. Lang, J. E. Mayer Jr, P. J. del Nido, and J. E. Lock Incorporation of the Hepatic Veins Into the Cavopulmonary Circulation in Patients With Heterotaxy and Pulmonary Arteriovenous Malformations After a Kawashima Procedure Ann. Thorac. Surg., November 1, 2005; 80(5): 1597 - 1603. [Abstract] [Full Text] [PDF]

				D. B. McElhinney, A. C. Marshall, P. Lang, J. E. Lock, and J. E. Mayer Jr Creation of a Brachial Arteriovenous Fistula for Treatment of Pulmonary Arteriovenous Malformations After Cavopulmonary Anastomosis Ann. Thorac. Surg., November 1, 2005; 80(5): 1604 - 1609. [Abstract] [Full Text] [PDF]

				M. Ono, N. Fukushima, H. Ichikawa, T. Ishizaka, Y. Sawa, and H. Matsuda Elevation of plasma angiotensin with the development of pulmonary arteriovenous malformations after cavopulmonary shunt J. Thorac. Cardiovasc. Surg., September 1, 2005; 130(3): 885 - 887. [Full Text] [PDF]

				B. W. Duncan and S. Desai Pulmonary arteriovenous malformations after cavopulmonary anastomosis Ann. Thorac. Surg., November 1, 2003; 76(5): 1759 - 1766. [Abstract] [Full Text] [PDF]