Pulmonary Hemodynamic responses to intravenous prostaglandin E-2 in broiler chickens

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 PGE2 at the lowest rate ( 30 mu g/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; PGE2: 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 30 +/- 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.