Influence of feed deprivation on ventilation and gas exchange in broilers: Relationship to pulmonary hypertension syndrome

被引:34
作者
Fedde, MR
Weigle, GE
Wideman, RF
机构
[1] Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA
[2] Univ Arkansas, Dept Poultry Sci, Fayetteville, AR 72701 USA
关键词
broiler; pulmonary hypertension syndrome; parabronchial ventilation; feed deprivation; hypoxemia;
D O I
10.1093/ps/77.11.1704
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
Fast-growing broiler chickens not uncommonly exhibit elevated pulmonary vascular resistance that leads to pulmonary hypertension and right ventricular failure. We tested the hypothesis that a distended gastrointestinal tract in these full-fed birds results in an abnormally low tidal 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 saturation of hemoglobin with oxygen (HbO(2)), O-2 consumption, and carbon dioxide elimination were measured on fast-growing broiler chickens when full-fed and after 3, 6, and 9 h of feed deprivation. Tidal volume of full-fed birds was not abnormally low despite HbO(2) values varying 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 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 hypoxemia. The data suggest that feed deprivation results in an increase in parabronchial ventilation, possibly from improvement in aerodynamic valving, which would reduce pulmonary hypoxic vasoconstriction and right ventricular failure. Tidal volume of full-fed birds was not abnormally low despite HbO(2) values varying 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 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 hypoxemia. The data suggest that feed deprivation results in an increase in parabronchial ventilation, possibly from improvement in aerodynamic valving, which would reduce pulmonary hypoxic vasoconstriction and right ventricular failure.
引用
收藏
页码:1704 / 1710
页数:7
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