Pulmonary and systemic hemodynamic responses to intravenous prostacyclin in broilers

The eicosanoid vasodilator prostacyclin (PGI(2)) reduces resistance to pulmonary blood flow and attenuates pulmonary hypertension in mammals. However, sparse information is available regarding the responsiveness of the avian pulmonary vasculature to PGI(2). Accordingly, in 3 experiments we evaluated the pulmonary vascular responses to PGI(2) in male broilers. In experiment 1, infusing PGI(2) (10 mug/min) into clinically healthy broilers did not reduce their pulmonary vascular resistance (PVR) but did reduce their pulmonary arterial pressure (PAP) by lowering their cardiac output. Within 4 min after stopping the PGI(2) infusion, the cardiac output and PAP returned to preinfusion levels. In experiment 2, the responses to PGI(2) were evaluated after arachidonic acid (AA) had been infused to preconstrict the pulmonary vasculature. The AA infusion (400 mug/min) consistently triggered dramatic, sustained pulmonary vasoconstriction (increased PVR) and pulmonary hypertension (increased PAP). Concurrent PGI(2) infusions did not reduce PVR but did reduce PAP by lowering cardiac output. Within 4 min after stopping the PGI(2) infusion, PAP and cardiac output returned to their previous (hypertensive) levels attributable to the ongoing AA infusion. In experiment 3, PGI(2) was infused (10 mug/min) into clinically healthy (PAP less than or equal to 24 mmHg) or subclinically hypertensive (PAP less than or equal to 27 mmHg) broilers. Throughout this experiment broilers in the hypertensive group had higher PAP values than broilers in the healthy group. The PGI(2) infusion reduced PAP in both groups but did not reduce PVR. Instead, the pulmonary hypotensive response to PGI(2) infusion was associated with a reduction in cardiac output in both groups. In all 3 experiments PGI(2) reduced PAP by reducing cardiac output rather than by reducing PVR. There was no evidence that PGI(2) acts as an effective pulmonary vasodilator in broilers regardless of whether their pulmonary vasculature was apparently normal (clinically healthy), had been pharmacologically preconstricted (AA infusion), or initially exhibited the vasoconstriction that is typical of the pathogenesis of pulmonary hypertension syndrome in broilers (PAP less than or equal to 27 mmHg). The consistent failure of PGI(2) to elicit pulmonary vasodilation in this study suggests fundamental differences in AA metabolism or the etiology of pulmonary hypertension may exist when broilers are compared with mammals.