Prostaglandin E(2) (PGE(2)) 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 PGE(2). Two experiments were conducted in which 45- to 55-d-old male broiler chickens were infused i.v. with PGE(2) at the lowest rate (30 mug/min for 4 min) that reliably reduced PAP during pilot studies. When compared with preinfusion (control) values in experiment 1, PGE(2) 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; PGE(2): 320 +/- 12 beats/min; P > 0.05). Infusing PGE(2) also reduced the RR from 57 +/- 2 to 46 +/- 4 breaths/min (P < 0.001) and reduced the percentage saturation of hemoglobin with oxygen (%HbO(2)) from 85 +/- 2 to 77 +/- 3%HbO(2) (P < 0.001). After the PGE(2) infusion ceased, the PAP, mean systemic arterial pressure, RR, and %HbO(2) 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, PGE(2) 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; PGE(2): 0.43 +/- 0.02 mL/kg of BW x beat; P = 0.158). After the PGE(2) 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 PGE(2) (control: 0.18 +/- 0.01 relative resistance units; PGE(2): 0.20 +/- 0.02 relative resistance units; P > 0.723). These results indicate that in broilers PGE(2) reduced PAP by reducing CO rather than by acting as a pulmonary vasodilator to lower PVR. The PGE(2)-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.