PubMed HealthSearch

PubMed · 2367265

Ascites in growing broilers: a research model.

Abstract

A method was developed to experimentally produce ascites in broiler chickens. High-altitude simulation (treatment group) was conducted to study the development of ascites in broiler chickens. In each of three experiments, 15 male broiler chicks (1 wk old) were placed in a hypobaric chamber (principal groups) for 5 wk and 15 other chicks were reared in batteries (control groups). Ascites occurred among chicks in the principal groups recorded at 13, 27, and 80% at simulated altitudes of 1,980, 2,438, and 2,896 m, respectively. No ascites were observed in the controls at 100 m (the altitude at College Station, Texas). Body weight was significantly (P less than .05) reduced for broilers in the principal groups versus the controls-especially at 2,896 m, where the principals weighed 500 g less than the controls. The counts for hematocrit, hemoglobin, and red blood cells were significantly (P less than .05) increased in all treatment groups; while at 2,438 and 2,896 m, corticosterone was significantly reduced. Histopathology indicated consistent, mild, cardiopulmonary lesions similar to those observed in the spontaneous ascites of broiler chickens. The high-altitude simulation model will be useful in studying the etiological factors and interactions causing ascites.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D A Witzel, W E Huff, L F Kubena, R B Harvey, M H Elissalde. 1990. Ascites in growing broilers: a research model.. https://doi.org/10.3382/ps.0690741

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Reemergence of spontaneous hypertension in hypoxia-protected rats returned to normoxia as adults.

Five-week-old male spontaneously hypertensive rats (SHR) were either exposed to hypoxia or maintained in normoxia. Groups of rats were returned to normoxia after 8 or 12 weeks exposure to hypoxia while others remained in hypoxia or normoxia throughout the study. Subdivisions of the groups were sacrificed 2 or 6 weeks after return to normoxia at the same time as were rats continuously exposed to either normoxia or hypoxia. Hypoxia attenuated the development of systemic hypertension (P less than 0.05); however, this protection dissipated partially when rats were returned to normoxia. Norepinephrine concentration was significantly elevated and serotonin turnover (5-hydroxyindoleacetic acid/serotonin 5HIAA/5HT) was significantly decreased in caudal brainstem of hypoxic SHR and both were gradually normalized upon return to normoxia. Similarly, left ventricular hypertrophy was attenuated and adrenal catecholamine contents were increased with hypoxic exposure. Both gradually normalized upon return to normoxia. Mechanisms associated with the development of spontaneous hypertension reemerge when adult, previously hypoxic SHR are returned to a normoxic environment. These findings implicate long-term changes in central noradrenergic and serotonergic function as components of the cardiovascular adaptation to hypoxia which includes hypoxic moderation of spontaneous hypertension.

Altitude