Cardio-pulmonary function in broilers reared at warm or cool temperatures: effect of acute inhalation of 100% oxygen
Fast growth and cool temperatures are the primary triggers for pulmonary hypertension syndrome (PHS, ascites) during commercial broiler growout. We evaluated cardio-pulmonary function in male broilers that initially were reared together at normal brooding temperatures and then were randomly assigned...
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Veröffentlicht in: | Poultry science 2000-02, Vol.79 (2), p.257-264 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Fast growth and cool temperatures are the primary triggers for pulmonary hypertension syndrome (PHS, ascites) during commercial broiler growout. We evaluated cardio-pulmonary function in male broilers that initially were reared together at normal brooding temperatures and then were randomly assigned to chambers maintained at 28 C (warm group) or 16 C (cool group). Cardio-pulmonary evaluations were conducted between 35 and 42 d of age. The groups initially did not differ in body weight, right:total ventricular weight ratio, respiratory rate, heart rate, total peripheral resistance, or pulmonary vascular resistance, nor did their arterial blood gas values differ for the partial pressure of carbon dioxide, bicarbonate concentration, or hydrogen ion concentration. When compared with the warm group, the cool group had heavier total ventricular weights and higher values for pulmonary arterial pressure, cardiac output, stroke volume, mean systemic arterial pressure, and hematocrit and a marginally lower (P = 0.06) partial pressure of oxygen. Inhaling 100% O2 for 20 min caused equivalent increases in the arterial partial pressure of oxygen (> or =388 mm Hg) and the percentage saturation of hemoglobin with oxygen (99.9%) in both groups. The respiratory rate was reduced and total peripheral resistance in both groups was increased; the pulmonary arterial pressure, cardiac output, and heart rate in the cool group were also reduced. Cool temperatures contributed to the increase in pulmonary arterial pressure primarily by increasing the metabolic demand for oxygen, as reflected by incipient hypoxemia (reduced blood oxygen and elevated hematocrit), generalized ventricular hypertrophy, and an elevated cardiac output. It was the elevated cardiac output rather than hypoxemic pulmonary vasoconstriction that increased the pulmonary arterial pressure in the cool group when compared with the warm group. |
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ISSN: | 0032-5791 |
DOI: | 10.1093/ps/79.2.257 |