In response to acute physical or psychological stress the circulating prolactin level rises (Noel et al 1972), a response that may be mediated by vasoactive intestinal peptide, oxytocin, dopaminergic pathways and/or other still uncharacterized factors; cytokines may also play a signalling role. Although prolactin appears to have immunostimulatory properties in animal models as well as in humans, it remains unclear whether the relative hyperprolactinaemia during the initial phase of critical illness or post-trauma contributes to the initial activation of the inflammatory cascade.

In the chronic phase of critical illness, serum prolactin levels are no longer as high as in the acute phase and the secretory pattern is characterised by a reduced pulsatile fraction (Fig. 1) (Van den Berghe et al 1998, Gardner et al 1979). A role for endogenous dopamine has been suggested. It is unknown whether the blunted prolactin secretion in the chronic phase plays a role in the anergic immune dysfunction or in the increased susceptibility for infections characterising the chronically ill (Meakins et al 1977). However, exogenous dopamine often infused as an inotropic drug in intensive care-dependent patients has been shown to further suppress prolactin secretion and was found to aggravate concomitantly both T lymphocyte dysfunction and impaired neutrophil chemotaxis (Van den Berghe 1994a).

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