INFLUENCE OF FEED DEPRIVATION ON VENTILATION AND GAS-EXCHANGE IN BROILERS - RELATIONSHIP TO PULMONARY-HYPERTENSION SYNDROME

Fast-growing broiler chickens not uncommonly exhibit elevated pulmonar y vascular resistance that leads to pulmonary hypertension and right v entricular failure. We tested the hypothesis that a distended gastroin testinal tract in these full-fed birds results in an abnormally low ti dal volume and minute ventilation that could lead to pulmonary hypoxia , pulmonary arterial vasoconstriction, right ventricular failure, and ascites. Tidal volume, respiratory frequency, heart rate, percentage s aturation of hemoglobin with oxygen (HbO(2)), O-2 consumption, and car bon dioxide elimination were measured on fast-growing broiler chickens when full-fed and after 3, 6, and 9 h of feed deprivation. Tidal volu me of full-fed birds was not abnormally low despite HbO(2) values vary ing from above 80% to nearly 60%. Importantly, HbO(2) was found to be markedly increased in the hypoxemic birds at and beyond a 3-h period w ithout feed, despite a reduction in minute ventilation. This response was not caused by a decrease in O-2 consumption. Thus, limitation of g as intake at the mouth was not the cause of the hypoxemia. The data su ggest that feed deprivation results in an increase in parabronchial ve ntilation, possibly from improvement in aerodynamic valving, which wou ld reduce pulmonary hypoxic vasoconstriction and right ventricular fai lure. Tidal volume of full-fed birds was not abnormally low despite Hb O(2) values varying from above 80% to nearly 60%. Importantly, HbO(2) was found to be markedly increased in the hypoxemic birds at and beyon d a 3-h period without feed, despite a reduction in minute ventilation . This response was not caused by a decrease in O-2 consumption. Thus, limitation of gas intake at the mouth was not the cause of the hypoxe mia. The data suggest that feed deprivation results in an increase in parabronchial ventilation, possibly from improvement in aerodynamic va lving, which would reduce pulmonary hypoxic vasoconstriction and right ventricular failure.