CHRONIC PAIN INDUCES A PARADOXICAL INCREASE IN GROWTH-HORMONE SECRETION WITHOUT AFFECTING OTHER HORMONES RELATED TO ACUTE STRESS IN THE RAT

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI). Using radio-immunoassay hormones were measured in plasma samples taken every 30 min for 7 h in free-moving rats 14 and 21 days after Freund adjuvant or vehicle injection and in control animals. The total amount of GH secretion was higher at 14 and 21 days PI in AIA rats as compared to vehicle-treated and control animals, and the pulsatility of GH secretory pattern was not modified by AIA. PRL and beta-END secretion were not significantly different in arthritic rats as compared to controls. These results show that GH, PRL and beta-END responses induced by acute stress are not observed during the AIA phase when chronic pain is maximum. Thus, in our experimental conditions, beta-END and PRL do not seem to be good plasma markers of chronic pain. The increase of GH secretion, at a stage of the illness when chronic pain is well developed, raises the questions of (1) the possible involvement of peptides, such as substance P or cytokines, released during chronic inflammatory painful syndromes in the regulation of pulsatile GH secretion, and (2) the possible involvement of a decrease in noradrenergic inhibitory inputs from the locus coeruleus exerted on GH secretion. The role of GH as a plasma marker of some aspects of chronic pain is a possibility that cannot be ruled out.