When pulmonary arterial blood flow is obstructed in all mammals studied, th
ere is a compensatory growth of the bronchial vasculature. This angiogenesi
s normally occurs through a proliferation of the systemic circulation to th
e intraparenchymal airways, It is an important pathophysiological process,
not only in pulmonary vascular disease, but also in lung cancer, because th
e blood how that supplies primary lung tumors arises from the systemic circ
ulation. In the mouse, however, the systemic blood vessels that supply the
trachea and mainstem bronchi do not penetrate into the intraparenchymal air
ways, as they do in all other larger species. In this study, we attempted t
o generate a new functional bronchial circulation in the mouse by permanent
ly obstructing 40% of the pulmonary circulation. We quantified the systemic
blood flow to the lung with fluorescent microspheres for 3 months after le
ft pulmonary artery ligation, Results demonstrated that a substantial syste
mic blood flow to the lung that can eventually supply up to 15% of the norm
al pulmonary flow can be generated beginning 5-6 days after ligation, These
new angiogenic vessels do not arise from the extraparenchymal bronchial ci
rculation. Rather they enter the lung directly via a totally new vasculatur
e that develops between the visceral and parietal pleuras, supplied by seve
ral intercostal arteries. This unique model of angiogenesis occurs in the a
bsence of any hypoxic stimulus and mimics the vascular source of many lung
tumors.