Changes in Pulmonary Arterial and Femoral Arterial Blood Pressure upon Acute Exposure to Hypobaric Hypoxia in Broiler Chickens

Abstract

An experiment was conducted to investigate the pulmonary arterial and femoral arterial pressure responses to acute hypobaric hypoxia. Twenty-four, 7-wk-old Hubbard x Hubbard male chickens were lightly anesthetized and catheters were introduced into the right femoral artery and the pulmonary artery. The birds were then placed in a hypobaric chamber, and blood pressure responses were monitored during acute (15 min) exposures to simulated altitudes of 2,000 and 4,000 m. The pulmonary artery pressure increased .7 and 4% during the first and second exposures to a simulated altitude of 2,000 m, whereas the femoral artery pressure decreased 6 and 8% during exposures to this altitude. The pulmonary artery pressure increased 7% on the first exposure and 23% (P < .05) on the second exposure to a simulated altitude of 4,000 m. The femoral arterial pressure decreased (P < .05) on both exposures to this altitude (29 and 24%, respectively). The initial femoral and pulmonary artery pressures and changes in these pressures upon exposure to hypobaric hypoxia were not consistently correlated with the characteristics of the electrocardiogram, packed cell volume, body weight, or the right:total ventricular weight ratio. These results indicate that acute hypobaric hypoxia elicits a hypotensive response in the systemic arterial circulation and a hypertensive response in the pulmonary arterial circulation of broiler chickens. Under the conditions of this experiment, indices known to be predictive of the onset of broiler pulmonary hypertension syndrome (BPHS) (increased electrocardiogram amplitude, increased packed cell volume, and increased right:total ventricular weight ratio) were not correlated with the magnitudes of femoral or pulmonary arterial pressure responses to hypobaric hypoxia, suggesting that major differences in the reactivity of systemic and pulmonary vascular beds could not be predicted by differences in BPHS indices within this population of clinically normal birds.