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Pulmonary Hemodynamic Responses to Intravenous Prostaglandin E₂ in Broiler Chickens

Department of Poultry Science, University of Arkansas, Fayetteville 72701

¹ Corresponding author: rwideman{at}uark.edu

Prostaglandin E₂ (PGE₂) affects pulmonary arterial pressure (PAP), pulmonary vascular resistance (PVR), and respiratory rate (RR) in mammals, but no information previously was available regarding avian pulmonary responses to PGE₂. Two experiments were conducted in which 45- to 55-d-old male broiler chickens were infused i.v. with PGE₂ at the lowest rate (30 µg/min for 4 min) that reliably reduced PAP during pilot studies. When compared with preinfusion (control) values in experiment 1, PGE₂ reduced PAP from 19 ± 1 to 16 ± 1 mmHg (P < 0.001) and reduced mean systemic arterial pressure from 111 ± 6 to 81 ± 5 mmHg (P < 0.001) but did not significantly reduce heart rate (HR; control: 338 ± 9 beats/min; PGE₂: 320 ± 12 beats/min; P > 0.05). Infusing PGE₂ also reduced the RR from 57 ± 2 to 46 ± 4 breaths/min (P < 0.001) and reduced the percentage saturation of hemoglobin with oxygen (%HbO₂) from 85 ± 2 to 77 ± 3%HbO₂ (P < 0.001). After the PGE₂ infusion ceased, the PAP, mean systemic arterial pressure, RR, and %HbO₂ recovered within 8 min to levels that did not differ from preinfusion control values. In experiment 2, an ultrasonic flow probe was surgically implanted on 1 pulmonary artery to measure cardiac output (CO). When compared with preinfusion control values, PGE₂ reduced CO from 140 ± 6 to 111 ± 5 mL/kg of BW x min (P < 0.001), reduced PAP from 25 ± 2 to 21 ± 1 mmHg (P < 0.001), and reduced RR from 49 ± 4 to 35 ± 4 breaths/min (P < 0.001). The reduction in CO was caused by a reduction in HR from 305 ± 9 to 260 ± 9 beats/min without a significant reduction in stroke volume (control: 0.46 ± 0.02 mL/kg of BW x beat; PGE₂: 0.43 ± 0.02 mL/kg of BW x beat; P = 0.158). After the PGE₂ infusion ceased the CO, PAP, RR, and HR recovered within 9 min to levels that did not differ from preinfusion control values. The PVR, calculated as PAP/CO, was not altered by PGE₂ (control: 0.18 ± 0.01 relative resistance units; PGE₂: 0.20 ± 0.02 relative resistance units; P > 0.723). These results indicate that in broilers PGE₂ reduced PAP by reducing CO rather than by acting as a pulmonary vasodilator to lower PVR. The PGE₂-induced reductions in PAP would benefit broilers that are susceptible to pulmonary hypertension syndrome by reducing their right ventricular overload; however, the reductions in CO and RR combined with the onset of systemic arterial hypoxemia would accelerate the pathophysiological progression leading to terminal pulmonary hypertension syndrome.

Key Words: respiration • pulmonary hypertension • cardiac output

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				R. F. Wideman, O. T. Bowen, and G. F. Erf Broiler pulmonary hypertensive responses during lipopolysaccharide-induced tolerance and cyclooxygenase inhibition Poult. Sci., January 1, 2009; 88(1): 72 - 85. [Abstract] [Full Text] [PDF]