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Complex Vascular Lesions in the Lungs of Domestic Fowl Selected for Susceptibility to Pulmonary Arterial Hypertension: Incidence and Histology
Author(s) -
Wideman Robert F,
Hamal K.,
Bayona M.,
Lorenzoni A.,
Cross D.,
Rhoads D.,
Erf G.,
Anthony N.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.572.8
Subject(s) - pathology , arteriole , pulmonary hypertension , muscle hypertrophy , lumen (anatomy) , medicine , histology , lung , microcirculation
Humans developing pulmonary arterial hypertension (PAH) have a poor prognosis for survival when plexiform lesions progressively obstruct their terminal pulmonary arterioles. Plexogenic arteriopathy rarely develops in existing animal models of PAH. Rapidly growing chickens spontaneously develop PAH accompanied by the formation of plexiform‐like complex vascular lesions (CVL). We now report the frequency with which at least one CVL per tissue section was observed in the lungs of chickens from a line selected for susceptibility to PAH: 48% of females (n = 128 lungs) and 44% of males (n = 132 lungs) spontaneously developed CVL; 38% of right lungs and 51% of left lungs exhibited CVL; and at 8, 12, 16, 20, 24, and 52 weeks of age the CVL incidences were 52, 50, 51, 40, 36, and 18%, respectively. CVL formed distal to branch points in muscular inter‐parabronchial pulmonary arterioles that typically exhibited medial hypertrophy and intimal proliferation. Perivascular mononuclear cell infiltrates consistently surrounded the affected arteriole branch points. Proliferating intimal cells fully or partially occluded the arteriole lumen adjacent to a mature CVL, and the dilated main body of the CVL encompassed diverse cell types, including foam‐like giant cells and a glomeruloid‐like capillary network. These CVL in the lungs of chickens strikingly resemble published photomicrographs of plexiform lesions in the lungs of human PAH patients, potentially providing biomedical researchers with a much‐needed animal model of spontaneous plexogenic arteriopathy. Supported by NIH grant 1R15HL092517.