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Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia Health System, Charlottesville, Virginia 22908
Pneumonectomy results in rapid
compensatory growth of the remaining lung and also leads to increased
flow and shear stress, which are known to stimulate endothelial nitric
oxide synthase (eNOS). Nitric oxide is an essential mediator of
vascular endothelial growth factor-induced angiogenesis, which should
necessarily occur during compensatory lung growth. Thus our hypothesis
is that eNOS is critical for compensatory lung growth. To test this,
left pneumonectomy was performed in eNOS-deficient mice (eNOS
/),
and compensatory growth of the right lung was characterized throughout
14 days postpneumonectomy and compared with wild-type pneumonectomy and sham controls. Compensatory lung growth was severely impaired in
eNOS/ mice, as demonstrated by significant reductions in lung
weight index, lung volume index, and volume of respiratory region.
Also, pneumonectomy-induced increases in alveolar surface density and
cell proliferation were prevented in eNOS/ mice, indicating that
eNOS plays a role in alveolar hyperplasia. Compensatory lung growth was
also impaired in wild-type mice treated with the nitric oxide synthase
inhibitor NG-nitro-L-arginine methyl
ester. Together, these results indicate that eNOS is critical for
compensatory lung growth.
angiogenesis; pulmonary regeneration; pneumocytes; alveolar proliferation
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