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J Thorac Cardiovasc Surg 2000;120:88-98
© 2000 The American Association for Thoracic Surgery

SURGERY FOR CONGENITAL HEART DISEASE

Systemic lobar shunting induces advanced pulmonary vasculopathy

From the Department of Surgery, University of Louisville,^a Louisville, Ky; the Department of Surgery, Division of Cardiothoracic Surgery,^b and the Department of Medicine and Cardiovascular Research Center, Medical College of Wisconsin,^c Milwaukee, Wis; the Department of Pediatrics, University of New Mexico,^d Albuquerque, NM; and the Research Service, Zablocki Veterans Administration Medical Center,^e Milwaukee, Wis.

Supported in part by grants from the Department of Veterans Affairs, Falk Trust, and National Institutes of Health grant HL 19298.

Address for reprints: Michael Bousamra, MD, Jewish Hospital Heart Lung Institute, 201 Abraham Flexner Way, Suite 1200, Louisville, KY 40241 (E-mail: bousamra{at}louisville.edu ).

Objectives: 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.

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