Regional hemodynamic effects of dopamine in the indomethacin-treated preterm infant

We have previously demonstrated that dopamine induces selective renal vasodilation without affecting cerebral and mesenteric blood flow in < or = 32 weeks' gestation normotensive preterm infants during the first postnatal day. In the present study, we have examined whether pretreatment with indomethacin affects the regional hemodynamic response to dopamine in >1-day-old normotensive preterm infants with similar gestational age.

The pulsatility index (PI) was used to assess the dopamine-induced changes in renal, mesenteric, and cerebral blood flow using color Doppler ultrasonography in 20 indomethacin-treated normotensive preterm neonates with patent ductus arteriosus (gestational age: 27.2+/-1.5 weeks; postnatal age: 35.7+/-8.2 hours). Dopamine (5 microg/kg per minute) was started 4.9+/-2.1 hours (range: 2 to 8 hours) after the first dose of indomethacin to combat oliguria and/or impaired peripheral perfusion. Blood flow velocity measurements were obtained immediately before and 10 minutes after the start of dopamine with each subject serving as his/her own control.

Dopamine increased heart rate and urine output but did not affect blood pressure at the dose applied. Dopamine decreased the PI in the renal and superior mesenteric artery (2.6+/-1.32 vs. 1.61+/-0.7 and 2.36+/-1.12 vs. 1.76+/-0.64, respectively; p<0.05) whereas the PI in the middle cerebral artery remained unchanged. These results are consistent with a dopamine-induced increase in renal and mesenteric blood flow without an effect on cerebral blood flow.

When started at least 2 hours after the first dose of indomethacin, dopamine induces renal and mesenteric vasodilation without affecting cerebral hemodynamics in the >1-day-old indomethacin-treated preterm infant.