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J Thorac Cardiovasc Surg 2004;127:1009-1017
© 2004 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Regression of postobstructive vasculopathy after revascularization of chronically obstructed pulmonary artery

^a Laboratoire de Chirurgie Expérimentale, Hôpital Marie Lannelongue, Université Paris Sud, Le Plessis Robinson, France
^b Department of Pathology, McGill University, Montreal, Quebec, Canada

Read at the Eighty-third Annual Meeting of The American Association for Thoracic Surgery, Boston, Mass, May 4-7, 2003.

Received for publication April 30, 2003; revisions received June 17, 2003; accepted for publication July 22, 2003.

^* Address for reprints: Elie Fadel, MD, Hôpital Marie Lannelongue, 133 Avenue de la Résistance, 92250, Le Plessis Robinson, France
fadel{at}ccml.com

OBJECTIVES: Pulmonary vascular resistance decreases dramatically after pulmonary thromboendarterectomy and further improves in time. This may reflect the slow regression of postobstructive pulmonary vasculopathy. We hypothesized that postobstructive pulmonary vasculopathy may regress after reperfusion in a piglet model of chronic (5 weeks) left pulmonary artery obstruction.

METHODS: The ligated left pulmonary artery was reimplanted into the pulmonary arterial trunk. Pulmonary artery blood flow and pressure were measured 2 days and 5 weeks after reperfusion. Pulmonary artery smooth muscle thickness, endothelium-dependent relaxation, and left lung endothelial nitric oxide synthase activity and expression were assessed 5 weeks after ligation (n = 10) and 5 weeks after reperfusion (n = 10), and compared with a sham group (n = 10). Patency of the anastomoses and systemic blood supply to the lung were assessed by pulmonary angiography and nonselective thoracic aortography, respectively.

RESULTS: Angiography showed that pulmonary artery anastomoses were patent in all animals. Five weeks after reperfusion, left pulmonary blood flows were similar to those in the sham animals, and systemic blood supply to the left lung decreased. Left pulmonary vascular resistance decreased by 50% at 5 weeks after reperfusion compared with 2 days after reperfusion (P = .0009). Medial muscle thickness of the left pulmonary artery greater than 600 µm increased 5 weeks after ligation and regressed to sham values 5 weeks after reperfusion (P = .001). Endothelium-dependent relaxation was only partially restored 5 weeks after reperfusion, whereas left lung endothelial nitric oxide synthase expressions and activities returned to sham values.

CONCLUSIONS: This study shows that postobstructive pulmonary vasculopathy induced by ligation of the pulmonary artery for 5 weeks regresses after reperfusion, accounting for the progressive improvement in hemodynamics after thromboendarterectomy.

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