title: Systemic lobar shunting induces advanced pulmonary vasculopathy.
abstract: OBJECTIVE
  We characterized the morphology and vasomotor responses of a localized, high-flow model of pulmonary hypertension.
  
  
  METHODS
  An end-to-side anastomosis was created between the left lower lobe pulmonary artery and the aorta in 23 piglets. Control animals had a thoracotomy alone or did not have an operation. Eight weeks later, hemodynamic measurements were made. Then shunted and/or nonshunted lobes were removed for determination of vascular resistance and compliance by occlusion techniques under conditions of normoxia, hypoxia (FIO (2) = 0.03), and inspired nitric oxide administration. Quantitative histologic studies of vessel morphology were performed.
  
  
  RESULTS
  Eighty-three percent of animals having a shunt survived to final study. Aortic pressure, main pulmonary artery and wedge pressures, cardiac output, blood gases, and weight gain were not different between control pigs and those receiving a shunt. Six of 9 shunted lobes demonstrated systemic levels of pulmonary hypertension in vivo. Arterial resistance was higher (24.3 +/- 12.0 vs 1.3 +/- 0. 2 mm Hg. mL(-1). s(-1), P =.04) and arterial compliance was lower (0. 05 +/- 0.01 vs 0.16 +/- 0.03 mL/mm Hg, P =.02) in shunted compared with nonshunted lobes. Hypoxic vasoconstriction was blunted in shunted lobes compared with nonshunted lobes (31% +/- 13% vs 452% +/- 107% change in arterial resistance, during hypoxia, P <.001). Vasodilation to inspired nitric oxide was evident only in shunted lobes (34% +/- 6% vs 1.8% +/- 8.2% change in arterial resistance during administration of inspired nitric oxide, P =.008). Neointimal and medial proliferation was found in shunted lobes with approximately a 10-fold increase in wall/luminal area ratio.
  
  
  CONCLUSIONS
  An aorta-lobar pulmonary artery shunt produces striking vasculopathy. The development of severe pulmonary hypertension within a short time frame, low mortality, and localized nature of the vasculopathy make this model highly attractive for investigation of mechanisms that underlie pulmonary hypertension.
authors.affiliation: Department of Surgery, University of Louisville, Louisville, KY. bousamra@louisville.edu
authors.forename: M
authors.initials: M
authors.lastname: Bousamra
authors.forename: R
authors.initials: R
authors.lastname: Rossi
authors.forename: E
authors.initials: E
authors.lastname: Jacobs
authors.forename: M
authors.initials: M
authors.lastname: Parviz
authors.forename: C
authors.initials: C
authors.lastname: Busch
authors.forename: L D
authors.initials: LD
authors.lastname: Nelin
authors.forename: S
authors.initials: S
authors.lastname: Haworth
authors.forename: C A
authors.initials: CA
authors.lastname: Dawson
mesh_terms: D000714:Anastomosis, Surgical / Q000009:adverse effects; D000818:Animals; D000831:Animals, Newborn; D001013:Aorta, Thoracic / Q000601:surgery*; D001157:Arterial Occlusive Diseases / Q000209:etiology; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D011651:Pulmonary Artery / Q000601:surgery*; D013552:Swine; D014656:Vascular Surgical Procedures / Q000009:adverse effects