PULMONARY ARTERIOLE HYPERTROPHY IN BROILERS WITH PULMONARY-HYPERTENSION SYNDROME (ASCITES)

Citation
B. Enkvetchakul et al., PULMONARY ARTERIOLE HYPERTROPHY IN BROILERS WITH PULMONARY-HYPERTENSION SYNDROME (ASCITES), Poultry science, 74(10), 1995, pp. 1677-1682
Citations number
31
Categorie Soggetti
Agriculture Dairy & AnumalScience
Journal title
ISSN journal
00325791
Volume
74
Issue
10
Year of publication
1995
Pages
1677 - 1682
Database
ISI
SICI code
0032-5791(1995)74:10<1677:PAHIBW>2.0.ZU;2-Q
Abstract
Two experiments were conducted to determine the effect of low ventilat ion or cool temperature environments on pulmonary arteriole hypertroph y. Male broilers were maintained under control or low ventilation cond itions in Experiment 1, whereas male broiler breeder by-product chicks were exposed to cool temperature conditions in Experiment 2. Birds we re randomly selected for histological evaluation of lung tissue in bot h experiments. In Experiment 1, birds that had pulmonary hypertension syndrome (PHS+) exhibited a greater degree of inflammation of lung tis sue at 5 and 7 wk of age than controls or birds that did not have PHS (PHS-). These PHS+ birds also had higher numbers of cartilaginous osse ous nodules at 3 and 7 wk of age than controls. Morphometric analyses revealed that PHS+ birds in Experiment 1 had a thicker medial layer as sociated with 100 to 200 mu m diameter pulmonary arterioles at 7 wk of age, and 50 to 100 mu m arterioles at 3 and 7 wk of age than PHS- or control birds. In Experiment 2, PHS+ birds exhibited a thicker medial layer in pulmonary arterioles at 7 wk of age than did PHS- birds, but there were no differences in medial layer thickness at 5 wk of age nor were there differences in the degree of inflammation or amount of oss eous nodule formation between PHS+ and PHS- birds at 5 and 7 wk of age , Thus, pulmonary arteriole hypertrophy was observed in birds having P HS in response to both low ventilation and cool temperature environmen ts and this hypertrophy occurred with or without a coincident inflamma tory response in lung tissue.