A sedative effect of dopamine on the respiratory burst in neonatal polymorphonuclear leukocytes.

Studies were performed to examine the effect of dopamine on the functions of neonatal polymorphonuclear leukocytes (PMN). Cord blood PMN were treated with dopamine and assayed for their superoxide anion production by the ferricytochrome C reduction method and for their myeloperoxidase-hypochlorous system ability by the luminol-dependent chemiluminescence using a synthetic chemotactic factor, N-formyl-methionyl-leucyl-phenylalanine, as a stimulus. Dopamine inhibited N-formyl-methionyl-leucyl-phenylalanine-induced O2- production by neonatal PMN: when PMN were treated with 10(-5) M and 10(-4) M dopamine, the percentage inhibition values were 51 and 71%, respectively. Dopamine also inhibited the luminol-dependent chemiluminescence. PMN mobility and bactericidal ability were not affected by dopamine. Therapeutic dopamine plasma levels (873.5 +/- 174.0 ng/mL, n = 13, mean +/- SEM) observed in sick infants corresponded with the in vitro dopamine concentrations to inhibit the respiratory burst. Dopamine may be one of the drugs useful for reducing the oxygen-induced tissue damage associated with PMN in neonatal intensive care patients.