title: Regression of postobstructive vasculopathy after revascularization of chronically obstructed pulmonary artery.
abstract: OBJECTIVE
  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 microm 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.
authors.affiliation: Laboratoire de Chirurgie Expérimentale, Hôpital Marie Lannelongue, Université Paris Sud, France. fadel@ccml.com
authors.forename: Elie
authors.initials: E
authors.lastname: Fadel
authors.forename: René P
authors.initials: RP
authors.lastname: Michel
authors.forename: Saadia
authors.initials: S
authors.lastname: Eddahibi
authors.forename: Renée
authors.initials: R
authors.lastname: Bernatchez
authors.forename: Guy-Michel
authors.initials: GM
authors.lastname: Mazmanian
authors.forename: Bruno
authors.initials: B
authors.lastname: Baudet
authors.forename: Philippe
authors.initials: P
authors.lastname: Dartevelle
authors.forename: Philippe
authors.initials: P
authors.lastname: Herve
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000378:metabolism / Q000503:physiopathology* / Q000601:surgery*; D002908:Chronic Disease; D003097:Collateral Circulation / Q000502:physiology; D004195:Disease Models, Animal; D006976:Hypertension, Pulmonary / Q000378:metabolism / Q000503:physiopathology; D008026:Ligation; D008168:Lung / Q000098:blood supply* / Q000378:metabolism / Q000503:physiopathology*; D008955:Models, Cardiovascular; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D011183:Postoperative Complications / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D011651:Pulmonary Artery / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D011652:Pulmonary Circulation / Q000502:physiology; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D013552:Swine; D016896:Treatment Outcome; D017540:Tunica Media / Q000378:metabolism / Q000503:physiopathology; D014654:Vascular Patency / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D014656:Vascular Surgical Procedures; D014664:Vasodilation / Q000502:physiology
chemical_list: D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III